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Parlodel

Generic Parlodel is the most effective preparation in struggle against female diseases as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Generic Parlodel can also be helpful for patients with Parkinson`s disease and its symptoms caused by low levels of dopamine in the brain. Generic Parlodel acts as up-to-date remedy reducing prolactin level.

Other names for this medication:

Similar Products:
Apokyn, Mirapex, Requip

 

Also known as:  Bromocriptine.

Description

Generic Parlodel is created using perfect medical formula which is a magnificent weapon against women problems such as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Target of Generic Parlodel is to reduce prolactin level and help to produce breast milk and fertility in women.

Generic Parlodel acts as up-to-date remedy reducing prolactin level. When it is used for treatment of Parkinson disease, it works by stimulating dopamine receptors in some certain brain parts.

Parlodel is also known as Bromocriptine, Proctinal.

Generic Parlodel is a hormone (dopamine agonist).

Generic Parlodel can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

Generic name of Generic Parlodel is Bromocriptine.

Brand name of Generic Parlodel is Parlodel.

Dosage

Generic Parlodel is available in the form of tablets (2.5 mg) which should be taken by mouth with meals or without it.

Take Generic Parlodel every day at the same time and remember that its dosage depends on patient's health state.

If you want to achieve most effective results do not stop taking Generic Parlodel suddenly.

Overdose

If you overdose Generic Parlodel and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store below 25 degrees C (77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Parlodel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Parlodel if you are allergic to Generic Parlodel components.

Do not take Generic Parlodel if you are pregnant, planning to become pregnant or breast-feeding.

Do not use Generic Parlodel in case of having uncontrolled high blood pressure, blood poisoning, having recently given birth or have coronary artery disease (chest pain) or any other severe heart disease.

In case you take Generic Parlodel while using birth control pills, remember that birth control pills become less effective

Patients under 15 years should be extremely careful with Generic Parlodel.

Avoid alcohol.

Be careful when you are driving machine.

It can be dangerous to stop Generic Parlodel taking suddenly.

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Reported cases of cyclical Cushing's syndrome are rare. Of 14 successive patients with Cushing's syndrome nine collected sequential urine samples for the estimation of cortisol:creatinine ratio. Five had cyclical Cushing's syndrome while two had considerable variation in urinary cortisol excretion without a cyclical pattern being established. Two of the five patients with a cyclical syndrome had paradoxical responses to dexamethasone. In only one patient with a cyclical pattern did the cortisol:creatinine ratio fall after treatment with bromocriptine or cyproheptadine, or both. The high incidence of the cyclical form of Cushing's syndrome has important clinical implications. A high index of suspicion of the syndrome is required in patients with symptoms or signs of Cushing's syndrome but with normal cortisol values, in patients with fluctuating cortisol values, and in patients with anomalous responses to dexamethasone. Because of possible variations in steroidogenesis the results of drug studies in Cushing's syndrome must be interpreted cautiously.

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Lipopolysaccharide (LPS) injection in mammals orchestrates the release of many proinflammatory and anti-inflammatory cytokines. Intravenous administration of 0.2 mg/kg of LPS into unanesthetized rats with indwelling jugular catheters provoked a rapid, 50-fold increase in plasma tumor necrosis factor (TNF)-alpha within 30 min, which declined by 60% by 120 min. To test our hypothesis that such a rapid increase of TNF-alpha would be either neurally or hormonally controlled, the effect on TNF-alpha release of anesthesia (ketamine/acepromazine/xylazine) and catecholaminergic agonists and antagonists, either alone or in the presence of LPS, was determined.

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Although cardiopulmonary adverse effects have been reported with the use of cabergoline (another dopamine agonist), to the best of our knowledge, this is the first case report of severe life-threatening DCMP associated with bromocriptine therapy. Causality assessment using the Naranjo probability scale revealed that the adverse drug event was probable.

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A 50 year old man with hyperthyroidism secondary to inappropriate secretion of TSH is described. On presentation T3 (42.1 nmol/L), T4 (265 nmol/L) and TSH (17.9 mU/L) were all markedly elevated. A diagnosis of a TSH-secreting pituitary tumor was suspected on the basis of a blunted TSH response to TRH and the absence of suppression of TSH by T3 or bromocriptine, but TSH/alpha subunit molar ratios were uncharacteristically less than 1. Nevertheless, the presence of a tumor was confirmed by computed tomography which demonstrated a 15 mm pituitary macroadenoma. The patient was treated with octreotide which resulted in normalisation of thyroid hormone levels. The duration of action of a single 100 micrograms injection of octreotide was at least 56 hours. The suppression of thyroid hormone levels was similar regardless of the treatment regimen with octreotide (100 micrograms tid, 250 micrograms bid, 100 micrograms bid and continuous subcutaneous infusion (CSI] and no escape was observed during a 16 month treatment period. TSH alpha subunit concentrations were also suppressed during long-term treatment with octreotide (3.3 micrograms/L falling to 1.1 micrograms/L), although no acute changes were noted after administration of single dose octreotide 100 micrograms. Three times the octreotide therapy was discontinued. The incremental rise in TSH and the maximum level of TSH achieved was less on each subsequent occasion, suggesting a suppressive effect of octreotide on the tumor itself. Despite suppression of TSH with octreotide over a 13 month period the pituitary tumor showed no shrinkage on repeat MRI scanning. In conclusion, this patient demonstrates that the differential diagnosis of inappropriate TSH secretion based only on biochemical test may be unreliable.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pergolide, along with bromocriptine and lisuride, is one of the most active dopamine receptor agonists. To determine whether or not pergolide protects against dopaminergic neuronal damage, via its activity on monoamine metabolism, we studied the effects of pergolide pretreatment on changes in monomaines and their metabolites in the mouse striatum after intracerebroventricular injection of 6-hydroxydopamine with pretreatment of desipramine. After intracerebroventricular administration of 6-hydroxydopamine (40 micrograms) in mice, the levels of dopamine and its metabolites (DOPAC, HVA) in the striatum rapidly decreased to 49%, 29% and 68%, respectively, of the naive controls at week 1 but then gradually recovered to control levels at weeks 2 and 4. Repeated pretreatment with pergolide (0.5 mg/kg, i.p.) for 7 days before administration of 6-hydroxydopamine, almost completely protected against reduction in striatal dopamine and its metabolites 1 week after injection of 6-hydroxydopamine. Therefore, pergolide could normalize the decreased dopamine synthesis or storage, and has a neuroprotective effect against dopaminergic dysfunction induced by the neurotoxin, 6-hydroxydopamine. Although we found that pergolide did not show radical scavenging activity in an in vitro system that generated hydroxyl radicals, it has been reported in vivo that pergolide treatment may induce Cu/Zn superoxide dismutase in the rat striatum. Considering these findings, pergolide may well be protective to dopaminergic neurons, largely because of its effects on presynaptic autoreceptors and on its induction of Cu/Zn superoxide dismutase. Further research on the neuroprotective effects of pergolide in Parkinson disease models, by injection of 6-hydroxydopamine, is needed to clarify its mechanism of action on dopaminergic indices.

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Declines in dopamine neurotransmission are a robust characteristic of the process of normal aging. Using neuroimaging, biochemical and cognitive methods, age-related reduction of D2 receptor has been noted in a wide range of species. On the other hand, it is well known that dopamine plays a crucial role in the modulation of sensory gating. Here, we examined age-related alterations of D2 receptor in rhesus monkeys, using a sensory gating paradigm. The direct D2 receptor agonist, bromocriptine, was characterized in young adult and aged monkeys. We found bromocriptine disrupted sensory gating in young adult monkeys but not in aged ones. Our results provided new evidence that there is a functional decline of D2 receptor in aged monkeys.

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The efficacy and tolerability of a slow-release preparation of bromocriptine (Parlodel SRO) were compared to those of conventional bromocriptine (Parlodel R) in a double blind, double dummy study of 12 hyperprolactinemic women (plasma PRL 81.3 +/- 4.73, ng/ml mean +/- SEM). For 2 weeks, the patients received 2.5 mg b.i.d. Parlodel R or 5 mg once daily Parlodel SRO; for the following 2 weeks, the dose of the drugs was doubled. The patients were then treated, in an open study, with 2.5-10 mg daily Parlodel SRO for 6 months. Both preparations caused a prompt and sharp PRL fall. Hormone levels remained inhibited over the whole month of observation with both preparations. Daily PRL profiles were very close with either drug although morning PRl levels were slightly higher during Parlodel SRO than during Parlodel R administration. Doubling the doses of the two drugs did not result in further significant lowering of PRL values. During the 6-month study with Parlodel SRO, plasma PRL further decreased and normalized in 11 of 12 patients. Clinical improvement occurred in the majority of cases. Tolerability of Parlodel SRO appeared to be better, though without statistically significant differences, than that of Parlodel R. Side effects were less important with the former compound in their number, severity and duration. In conclusion, thanks to its favourable pharmacological profile, Parlodel SRO appears to be a valuable alternative to regular bromocriptine in the management of hyperprolactinemia.

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Circulating PRL influences the progression of DR after its intraocular conversion to vasoinhibins. Inducing hyperprolactinemia may represent a novel therapy against DR.

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In 15 hyperprolactinaemic, infertile patients achieving 17 bromocriptine-induced pregnancies, the presence or absence of prolactin (Prl) increment in the 3rd trimester of pregnancy was correlated to the basal Prl levels before treatment and after pregnancy. The hyperprolactinaemic patients revealed a marked heterogeneity in the Prl increment compared to normal women. Five patients showed a pronounced increase in serum Prl during gestation, whereas Prl levels were unaltered or decreased slightly in 10 patients. In the latter group of patients serum Prl was significantly (P less than 0.01) lower after pregnancy than before treatment. Our study indicates that some hyperprolactinaemic patients may benefit from a pregnancy, and that these patients probably can be identified, as they do not show any significant changes in Prl levels during pregnancy.

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In order to clarify endocrine abnormalities due to hypothalamic involvement in multiple sclerosis (MS), serum prolactin levels were measured in 27 patients with MS and 22 healthy subjects. The presence of hypothalamic lesions was also studied by magnetic resonance imaging (MRI). Serum prolactin levels were found to be significantly higher in MS patients than in healthy controls in both sexes. Although only one patient had galactorrhea, one-third of the MS patients had mild to moderate hyperprolactinemia, which was a 4-13-fold increase over the mean value of healthy subjects. The results of thyrotropin-releasing hormone, sulpiride, L-DOPA and bromocriptine loading tests suggested a hypothalamic dysfunction, rather than pituitary prolactinoma in MS patients. Four of eight patients with hyperprolactinema had diencephalic hypothalamic lesion(s) contiguous with the third ventricle on the brain MRI, while none of the normoprolactinemic patients had any lesions in the diencephalon. All relapsing-remitting patients with hyperprolactinemia showed a rise in prolactin levels in the acute stage of the relapse and a decrease during the recovering stage and the following remission phase. Our findings suggest that latent hyperprolactinemia due to hypothalamic dysfunction occurs frequently in MS patients in relapse. The increase of serum prolactin is considered to be a sensitive indicator for hypothalamic lesions in MS.

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Bromocryptine potently decreased prolactin (PRL) secretion of pituitary glands of 2-day-old rats in vitro (up to 85% inhibition; ED50 between 0.1 and 1.0 nM) without altering the bioactivity to immunoreactivity (B/I) ratio. Bromocryptine tended to suppress growth hormone (GH) secretion although the effect did not reach statistical significance. Angiotensin-II (A-II; 1-1000 nM) stimulated PRL secretion in a dose-dependent manner without affecting secretion of GH. The B/I ratio of PRL secreted in response to A-II was increased. Somatostatin (SRIF) had no effect on PRL secretion but inhibited GH secretion in a dose-dependent manner; significant inhibition (50%) was observed at 100 nM. A 6-h exposure to ovine PRL (oPRL) in concentrations equipotent with 1.2-120 ng/ml rat PRL (rPRL) in the Nb2 bioassay had no effect on immunoreactive rPRL secretion. Salmon calcitonin (sCT) and endothelin-3 (ET-3; 0.1-100 nM) failed to inhibit secretion of PRL or GH. PRL secretion was slightly stimulated by sCT with no apparent dose-response relationship. The present findings suggest that neonatal pituitary glands do not display autoregulation of PRL secretion, and sCT and ET-3 (either endogenous or milk-derived) may not function as PRL inhibiting factors in 2-day-old pups. Thus, the receptors of PRL, sCT and ET-3 on lactotropes, or their functional coupling with inhibition of basal PRL secretion, occur at a later stage of development. The specificity of the PRL releasing factor (PRF) activity of A-II at this age is unique for established PRFs and might reflect a physiological function of PRL in osmoregulation. The increased B/I ratio of PRL secreted in response to A-II may be due to the release of specific PRL variants, and might be a sign of functional heterogeneity among lactotropes. The differential sensitivity of PRL and GH to the applied secretagogues suggests that the intracellular regulation of PRL and GH are compartmentalized in the mammosomatotrope cell.

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Resonance Raman (RR) spectroscopy is used to help define active site structural responses of nanodisc-incorporated CYP3A4 to the binding of three substrates: bromocriptine (BC), erythromycin (ERY), and testosterone (TST). We demonstrate that nanodisc-incorporated assemblies reveal much more well-defined active site RR spectroscopic responses as compared to those normally obtained with the conventional, detergent-stabilized, sampling strategies. While ERY and BC are known to bind to CYP3A4 with a 1:1 stoichiometry, only the BC induces a substantial conversion from low- to high-spin state, as clearly manifested in the RR spectra acquired herein. The third substrate, TST, displays significant homotropic interactions within CYP3A4, the active site binding up to 3 molecules of this substrate, with the functional properties varying in response to binding of individual substrate molecules. While such behavior seemingly suggests the possibility that each substrate binding event induces functionally important heme structural changes, up to this time spectroscopic evidence for such structural changes has not been available. The current RR spectroscopic studies show clearly that accommodation of different size substrates, and different loading of TST, do not significantly affect the structure of the substrate-bound ferric heme. However, it is here demonstrated that the nature and number of bound substrates do have an extraordinary influence on the conformation of bound exogenous ligands, such as CO or dioxygen and its reduced forms, implying an effective mechanism whereby substrate structure can impact reactivity of intermediates so as to influence function, as reflected in the diverse reactivity of this drug metabolizing cytochrome.

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Extracellular single-cell recording and microiontophoretic techniques were used to characterize the presynaptic dopamine (DA) receptors (autoreceptors) on A10 DA neurons in the rat ventral tegmental area. Thus, the ability of various agonists to inhibit the activity of A10 DA neurons was compared. DA and the DA agonists N-n-propylnorapomorphine (NPA), apomorphine, lisuride, pergolide, LY141865 and bromocriptine all suppressed the activity of A10DA neurons. NPA was the most potent exogenous agonist, exerting effects that were similar to an equimolar concentration of DA (0.01 M). When ejected at equimolar concentrations (0.01 M) and equivalent ejection currents, the rank order of potency for these agonists was DA = NPA greater than LY141865 greater than pergolide = lisuride = apomorphine greater than norepinephrine greater than bromocriptine. The alpha-2 adrenoceptor agonist clonidine, the beta adrenoceptor agonist isoproterenol, the D-1 specific DA agonist SKF 38393 and the hallucinogenic ergot lysergic acid diethylamide exerted only weak effects or were inactive. The D-2 specific DA antagonist sulpiride completely blocked the rate-suppressant effects of DA and DA agonists but not those of gamma-aminobutyric acid. The purported D-1 specific DA antagonist SCH 23390 failed to block the effects of either DA or the D-2 specific DA agonist LY141865. These results indicate that DA agonists suppress the activity of the majority of A10 DA neurons by acting directly on somatodendritic DA autoreceptors which exhibit the pharmacological characteristics of D-2 receptors.

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9 females with microprolactin-secreting and 4 females with macroprolactin-secreting adenoma of the anterior lobe of the hypophysis (mean age 33.8 +/- 3.7 years) were examined using radioimmunoassay of the hormones, computed tomography, MR-tomography of the adrenals and brain.

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Two types of rat pituitary tumour cells secreting both prolactin (Prl) and growth hormone (GH) were cultured in vitro either on plastic dishes or on surfaces coated with an extracellular matrix (ECM) derived from bovine corneal endothelium. The presence of ECM caused an increase in Prl but a decrease in GH. On one cell line the Prl response to thyrotrophin releasing hormone (TRH) was increased by ECM. There was an increase in the rate of spread of the cultures, an increase in cell protein, and DNA synthesis and a change in cell morphology when ECM was used. It is suggested that these observations can be explained by a sensitizing action of ECM to growth factors present in serum.

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University hospital.

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The effect of six dopamine agonists including apomorphine, epinine, dopamine, piribedil, lergotrile and bromocriptine on the incorporation of [3H]tyrosine into dopamine was studied in slices and synaptosomes prepared from various brain areas containing dopamine terminals including striatum, nucleus accumbens, olfactory tubercle and medial basal hypothalamus. It was observed that all of these drugs were active in causing a decrease in dopamine synthesis in these various brain areas. The catecholamine agonists apomorphine, epinine and dopamine were more potent in inhibiting dopamine synthesis in the mesolimbic structures than in the striatum. On the other hand, apomorphine and epinine were less potent while dopamine was more potent in the medial basal hypothalamus. The ergoline drugs were weak agonists in all structures studied. It is concluded that autoreceptor regulation of dopamine synthesis is more active in the mesolimbic compared with the nigrostriatal dopamine pathway while autoreceptors may be absent in the median eminence.

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In a previous study, the authors demonstrated that meningioma cells secrete platelet-derived growth factor (PDGF)-like molecules that stimulate their own growth in an autocrine manner. Based on that finding, a study was undertaken to examine the effect of trapidil, a drug known to have an antagonistic action against PDGF, on cell proliferation of human meningiomas in culture. Trapidil showed a dose-dependent inhibition of meningioma cell proliferation in the absence of any exogenous mitogenic stimulation. The maximum effect was observed at a concentration of 100 micrograms/ml, with the decrease in cell growth ranging from 16% to 54% compared to control samples. Trapidil similarly inhibited the basal deoxyribonucleic acid (DNA) synthesis assessed by [3H]-thymidine incorporation in three of seven meningiomas. While the conditioned medium generated from meningioma cells remarkably stimulated the proliferation of meningioma cells (166% to 277% of control), this effect was strikingly inhibited by the addition of trapidil. Trapidil also inhibited conditioned medium-stimulated DNA synthesis, even when there was no effect on basal DNA synthesis. Furthermore, trapidil significantly inhibited the epidermal growth factor (EGF)-stimulated proliferation of meningioma cells. This inhibitory effect on EGF-stimulated cell proliferation was also observed in nontumorous fibroblasts, demonstrating that trapidil is not an antagonist specific to PDGF. The addition of trapidil (30 micrograms/ml) in combination with bromocriptine (1 microM) showed an additive inhibitory effect on the meningioma cell growth compared to trapidil or bromocriptine alone. The overall results suggest that trapidil exhibits an inhibitory effect on meningioma cell proliferation through blocking the mitogenic stimulation induced by autocrine or exogenous growth factors, and may be considered as a possible new approach to the medical treatment of meningiomas.

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Previous studies on the efficacy of bromocriptine for the treatment of patients with the polycystic ovary syndrome failed to include control groups. This study, therefore, was undertaken to determine the clinical and endocrine effects of bromocriptine and a placebo (given in a random double blind fashion) in 55 patients with PCOS. The plasma levels of estrone, estradiol, testosterone, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, and serum PRL and gonadotropins (LH and FSH) were measured before treatment. In addition the serum PRL response to TRH and the serum LH and FSH response to GnRH were determined. The effects of acute administration of bromocriptine (2 X 2.5 mg at 12-h intervals) on serum gonadotropins and their response to GnRH were studied to explore the possibility that this test might predict the response to chronic bromocriptine treatment. Bromocriptine then was given at an initial dose of 1.25 mg twice daily. If no clinical improvement occurred 2.5 mg were given twice daily for at least 6 months. Hormonal measurements and dynamic tests were repeated after 3 and 6 months of therapy. The endocrine profile of the two groups was not different before treatment. The clinical results were not better in the treatment group than in the placebo-treated patients: therapy was successful (restoration of ovulatory cycles of less than 35 days duration) in 12 of 28 patients taking bromocriptine vs. 8 of 27 taking placebo. Slight improvement (1 or 2 ovulations) occurred in 3 of 28 vs. 3 of 27, and failure (no clinical change) in 13 of 28 taking bromocriptine vs. 16 of 27 taking placebo, respectively. Serum PRL fell significantly in the bromocriptine group, and there was a significant fall in the serum LH response to GnRH in both groups. No hormonal measurement or response predicted the clinical response to treatment. The only significant effect of chronic bromocriptine therapy (5 mg/day) in patients with the polycystic ovary syndrome was to lower the serum PRL concentration.

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The possibility that dopamine may play a role in the in vivo control of aldosterone production in man was suggested to us by reports from others; (a) that bromocriptine, a dopaminergic agonist, inhibits the aldosterone response to diuresis and to the infusion of angiotensin or ACTH; and (b) that metaclopramide, a dopamine blocking agent, causes elevations in plasma aldosterone levels. To determine whether such effects were direct or indirect, we examined the action of dopamine on aldosterone biosynthesis in isolated, bovine adrenal cells. Dopamine significantly inhibits the aldosterone response to angiotensin (P < 0.001), but does not influence basal aldosterone biosynthesis. It has previously been reported that angiotensin stimulates both the early and late phases of aldosterone biosynthesis. The present experiments demonstrated that the enhancing effect of angiotensin on the conversion of deoxycorticosterone to aldosterone (late phase of aldosterone biosynthesis) was almost completely inhibited by dopamine (P < 0.001). A significant inhibitory effect of dopamine (10 nM) was seen even when aldosterone biosynthesis was stimulated by a grossly supraphysiological concentration of angiotensin II (10 muM). However, these studies did not demonstrate any direct effect of dopamine on the early phase of aldosterone biosynthesis (cholesterol to pregnenolone) basally or when stimulated, or on the late phase of aldosterone biosynthesis under basal conditions. These in vitro studies suggest a direct inhibitory role for dopamine on the late phase of aldosterone biosynthesis, which may account for the in vivo inhibition of the aldosterone response to angiotensin in subjects treated with a dopaminergic agent.

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To review the recommended management of pituitary tumors that occur in pregnant patients.

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To evaluate the effectiveness and safety of interventions used for suppression of lactation in postpartum women (who have not breastfed or expressed breastmilk) to determine which approach has the greatest comparative benefits with least risk.

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Activation of dopamine D(2)R by bromocriptine reverses enhanced diurnal TSH secretion in obese women. Thus, reduced dopaminergic neuronal signaling might be involved in the perturbation of the thyrotrope hormonal axis in obese premenopausal women.

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Twelve patients with acromegaly were treated with bromocriptine for periods from nine to 23 months. All showed some clinical improvement. There was no significant difference in plasma growth hormone levels before and after therapy with bromocriptine, but a significant fall in plasma prolactin levels was observed after the bromocriptine therapy was commenced. The release of other pituitary hormones was not affected by bromocriptine.

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Electronic searches of Cochrane Library, EMBASE, MEDLINE, PsycLIT, Biological Abstracts and LILACS; reference searching; personal communication; conference abstracts; unpublished trials from pharmaceutical industry; book chapters on treatment of cocaine dependence, was performed for the primary version of this review in 2001. Another search of the electronic databases was done in December of 2002 for this update. The specialised register of trials of the Cochrane Group on Drugs and Alcohol was searched until February 2003.

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Small pellets loaded with apomorphine, thyrotropin-releasing hormone, and bromocriptine were implanted into the right striatum of 6-hydroxydopamine-treated rotation rats, and the efficacy of this drug delivery system was examined. Pellets containing neuromodifying agents, when implanted into the brain, may be just as effective as brain grafting in delivering various chemical agents to the brain. This method is much safer and simpler than brain grafting, since it bypasses many of the complicated problems associated with brain grafting. Application of this method to an animal experimental model for brain grafting and possibly in the treatment of parkinsonism should be considered along with brain grafting.

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Bromocriptine therapy normalizes prolactin levels and restores fertility in 82 to 90% of patients with prolactinoma. Tumour diameter is reduced (> 25%) in 60 to 79% of patients within 3 to 12 months. Symptoms return in the majority of cases, even after 1.5 to 10 years of treatment, if the drug is withdrawn; thus, in macroprolactinoma, life-long dopamine agonist treatment is indicated. A depot formulation of bromocriptine has been introduced which allows 50 to 100 mg of bromocriptine to be administered at monthly intervals. Treatment resulted in normalization of prolactin levels in 72% of cases and a tumour shrinkage (> 25%) was noted in 54%. This preparation is well tolerated, apart from initial injection. CV 205-502 is a non-ergot long-acting dopamine agonist. A daily dose of 75 to 400 micrograms reduced hyperprolactinaemia in 58 to 91% of patients and induced tumour shrinkage in 52%. CV 205-502 achieved normal prolactin levels in 50% of patients previously diagnosed as bromocriptine-resistant. Cabergoline is an ergot derivative. A twice weekly dose of 0.2 to 3.5 mg induced tumour shrinkage in 96% of patients treated. Pergolide is another potent dopamine agonist and is expected to give similar results to cabergoline and CV 205-502.

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Bromocriptine suppressed lactation by depressing the serum prolactin (PRL) level in 10 of 12 cases with profuse galactorrhea. The PRL level in galactorrhea milk was lower than in serum and was similar to that obtained in normal mature milk. However, significantly higher total solid, total ash, lipid and calcium levels, and reduced lactose and potassium levels were seen in galactorrhea specimens compared to mature milk. Although all the constituents decreased during treatment, the highly significant reduction in lipid and calcium levels shows the predominant effect of PRL on mammary synthesis and/or transport of these constituents. Fasting serum total lipids, total cholesterol and triglyceride levels were significantly higher in the galactorrhea group than in breast-feeding women with established lactation, suggesting that elevated serum PRL plays a role in lipid metabolism.

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parlodel drug uses 2016-05-25

The management of CSF rhinorrhoea following dopamine agonist (DA) treatment for invasive prolactinomas is difficult and there is no clear consensus for its treatment. Our objective was therefore to investigate the different treatments for buy parlodel this condition.

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The sympathetic adrenal (SA) activity can be modulated by dopamine (DA) through D2 receptors. In man, using D2 antagonists, it has been demonstrated that endogenous DA plays an inhibitory modulation of the SA system during high degree of SA activation. D2 agonists are able to induce a decrease in norepinephrine (NE) release either in vitro or in vivo. This effect leads, in vivo, to a decrease in blood pressure (BP) and to an activation of arterial baroreceptors. Therefore, in vivo, the D2 mediated inhibition of epinephrine (E) release, which is clearly demonstrated in vitro, is overwhelmed by the baroreceptor-mediated activation of the splachnic nerve. As a consequence, the in vivo administration of D2 agonists can induce a different effect on the net peripheral sympathetic tone of an organ, depending on the balance between the degree of the baroreceptor-mediated sympathetic activation and the inhibitory D2-mediated inhibition of NE release at the tissue level. In the present paper we investigated the in vivo effect of placebo (PL) or acute oral bromocriptine (BC) administration on plasma CA and on the cardiac sympatho-vagal balance of 7 normal volunteers, as assessed by power spectral analysis of heart rate (HR) variability (autoregressive method), either in resting or sitting position. Low frequency (LF) and high frequency (HF) components, both expressed in normalized units (nU), and LF/HF ratio were calculated. BC caused a decrease in BP, plasma NE and no change in HR in resting and sitting position. Plasma E increased in sitting position. At the heart level, after BC, we observed, during rest, an increase in LF and LF/HF ratio and a decrease in HF while in sitting position LF did not increase further. These data show that BC, while reducing BP through a decrease of plasma NE, increases LF/HF ratio (sympathetic tone) without any change in heart buy parlodel rate. These data seem to confirm that BC causes an inhibitory modulation of the SA system acting predominantly at the periphery through D2 presynaptic receptors.

parlodel 1 mg 2015-08-15

In males, pretreatment prolactin levels were 71 362+/-29 912 mU/l while leptin levels were 14.9+/-1.8 microg/l. In females, pretreatment prolactin levels were 11 395+/-5839 mU/l and leptin levels were 16.7+/-2.5 microg/l. The sexual dimorphism of serum leptin levels at initial presentation was preserved after adjusting for BMI and prolactin-induced hypogonadism. After 1 month of therapy buy parlodel , prolactin levels significantly decreased (males: 17 618+/-8736 mU/l, females: 3686+/-2231; P<0.05), BMI did not change (males: 30.2+/-1.7 kg/m(2), females: 24.1+/-1.2 kg/m(2); P>0.05), while serum leptin levels decreased (males: 12.5+/-1.5 microg/l, females: 13.6+/-2.1 microg/l; P<0.05). After 6 months of treatment, prolactin further decreased (males: 3456+/-2101 mU/l, females: 677+/-360 mU/l; P<0.05) as did BMI (males: 28.6+/-1.6 kg/m(2), females 23.1+/-1.0 kg/m(2); P<0.05). The difference was more pronounced in male patients. Leptin levels were 12.8+/-2.8 microg/l in males and 12.9+/-1.8 microg/l in females (P<0.05). After 2 years of BC treatment, prolactin levels were near normal (males: 665+/-439 mU/l, females 447+/-130 mU/l; P<0.05) and BMI remained 26.5+/-1.9 kg/m(2) for males and 23.6+/-0.8 kg/m(2) for females (P<0.05). Leptin levels were 9.5+/-2.2 microg/l in males and 18.7+/-3.1 microg/l in females (P<0.05). There was a gradual increase in the gender difference in serum leptin levels over time. Changes in serum leptin levels significantly correlated with changes in BMI (r=0.844, P<0.001) but did not correlate with changes in plasma prolactin levels after 1 month (r=0.166), 6 months (r=0.313) and 2 years (r=0.234, P>0.05).

parlodel tabs 2016-01-20

The introduction of radioimmunoassay for prolactin concentrated interest in infertility research on prolactin-producing pituitary adenomas (prolactinomas). In women in the fertile age group these tumors cause amenorrhea and galactorrhea, and in men loss of libido, impotence and occasionally gynecomastia. Microprolactinomas (diameter 10 mm and less) and macroprolactinomas (diameter more than 10 mm) differ in growth characteristics, symptomatology and prognosis. Different therapeutic approaches may be used. Both bromocriptine treatment and selective microsurgical tumor extirpation are successful. Both have advantages and disadvantages, thus rendering the decision as buy parlodel to appropriate treatment increasingly difficult. Recent findings demonstrate that bromocriptine may cause irreversible tumor fibrosis, which decreases the chances of prolactin normalization by subsequent surgery.

parlodel and alcohol 2017-04-06

Dopamine agonist buy parlodel therapy in patients with NFPA is associated with decreased prevalence of residual tumor enlargement after transsphenoidal surgical resection.

parlodel reviews 2016-04-12

Forty-two patients with elevated serum prolactin were treated in a randomized, open-label trial with the conventional ergot bromocriptine, or a new ergot pergolide. Before treatment, the patients underwent thorough endocrine evaluation and computed tomographic scan. All patients had prolactin levels greater than 25 ng/ml, and 27 patients had a pituitary mass. Follow-up studies performed after 6 months of treatment showed both drugs effectively reduced prolactin levels to normal, though pergolide effects were more rapid. There was no change in the contents of the pituitary fossa in the 10 patients with hyperprolactinemia but without pituitary mass. Sixty percent of patients with pituitary mass had diminution of tumor size. Pergolide appears to be an effective medical treatment for hyperprolactinemia and pituitary tumor and offers a possible alternative to bromocriptine and buy parlodel surgical treatment.

parlodel drug 2017-01-13

This report experimentally examined whether the genetically determined low nigrostriatal/mesolimbic dopaminergic activity in the C57BL/6J (herein referred to as C57) inbred mouse mediated the congenital high risk for ethanol abuse (ethanol consumption and ethanol preference) in this model. C57 mice pretreated with dopamine D1 receptor agonist ((+)-SKF-38393) or dopamine D2 receptor agonist (bromocriptine) to augment synaptic dopamine availability exhibited marked 76% and 38% reductions in voluntary ethanol intake in comparison to untreated controls. Dopamine receptor agonist administration resulted in changes in dopamine D1 and D2 receptor mRNA in the cell bodies and dopamine D1 and D2 receptor densities principally in the afferent targets of nigrostriatal/mesolimbic dopamine neurons. Dopamine receptor agonists promoted a decrease of striatal dopamine D1 and D2 receptor densities and corresponding down-regulation of olfactory tubercle dopamine D1 and D2 receptor mRNA abundance. Dopamine receptor agonist-induced increases in forebrain dopaminergic activity was compensated with increased dopamine D2 receptor density and correspondingly higher dopamine D2 receptor mRNA content in the brain stem. When bromocriptine was administered to ethanol-sensitized mice, it was ineffective in reducing voluntary ethanol abuse. buy parlodel In these mice, treatment with the dopamine D2 receptor antagonist haloperidol led to a 28% reduction in the absolute amount of ethanol consumed, but not in voluntary ethanol preference. These data indicated that nigrostriatal/mesolimbic dopamine D1-D2 receptor mechanism(s) mediating the potential for becoming high ethanol drinking on exposure to ethanol are distinct from factors mediating voluntary ethanol drinking after sensitization to ethanol. These data constitute direct evidence supporting a dopamine hypothesis for ethanol abuse in the genetically ethanol-preferring C57 mouse.

parlodel tab 2015-05-06

In this large-scale retrospective study buy parlodel , the medical treatment of mild hyperprolactinemia was shown to be effective and sufficient after 9 years of follow-up.

parlodel generic 2016-10-20

7% of our Chinese PD subjects had impulse control disorders. When young Parkinson's disease patients with a history of anxiety or depression are treated with high dose of DA, they are at risk of buy parlodel developing impulse control disorders.

parlodel user reviews 2017-09-14

A behavioral study was performed in an attempt to understand the neuronal mechanisms involved in yawning behavior in rats. Subcutaneous injections of low doses of apomorphine (0.05-0.25 mg/kg) or piribedil (0.2-1.0 mg/kg), which preferentially activate presynaptic dopamine autoreceptors at those doses, evoked yawning. Marked yawning responses were also elicited by both 3-PPP (5-20 mg/kg, SC) and TL buy parlodel -99 (1-2 mg/kg, SC). SK & F 38393, a dopamine D-1 receptor agonist, at doses ranging from 0.1 to 8.0 mg/kg (SC) induced neither yawning nor stereotypy. However, bromocriptine (0.5-32.0 mg/kg, SC), a dopamine D-2 receptor agonist, induced yawning for which the dose-response curves showed a bell-shaped form. After a higher dose of 32 mg/kg (SC) bromocriptine, some rats occasionally showed sniffing and sawdust chewing. Yawning responses induced by systemic injection of apomorphine, piribedil, 3-PPP or bromocriptine were wholly suppressed after treatment with sulpiride (10 mg/kg SC), a dopamine D-2 receptor antagonist. Bilateral injections of apomorphine (20 micrograms/side X 2), piribedil (100 micrograms/side X 2) or 3-PPP (50, 100 micrograms/side X 2) into the striatum or septum also elicited marked yawning. The results indicate that low doses of apomorphine, piribedil, 3-PPP, TL-99 or bromocriptine elicit yawning by stimulating dopamine D-2 receptors and striatal and septal dopaminergic systems may be related to the occurrence of yawning behavior.

parlodel ovulation drug 2015-12-12

The aim of this study was to examine prolactin (PRL) regulation of preproenkephalin and proopiomelanocortin (POMC) gene expression in the hypothalamus during lactation. In the first experiment, lactating rats were deprived of pups for 3, 6, 12, or 24 h. Preproenkephalin mRNA levels were decreased in the arcuate nucleus (ARC) to 60 or 53% of suckled levels and in the ventromedial nucleus to 70% of suckled levels after 12 or 24 h but were unchanged in the striatum. POMC mRNA levels in the ARC and periarcuate area were increased to 165% of suckled levels within 3 h and remained elevated two- to threefold for 24 h. Subcutaneous administration of bromocriptine to suckled dams markedly suppressed circulating PRL levels and decreased preproenkephalin mRNA signal levels to 38 and 50% of control levels in the arcuate and ventromedial nuclei, respectively. Intravenous administration of oPRL completely reversed this effect. By contrast, bromocriptine with or without administration of ovine PRL (oPRL) did not alter POMC mRNA signal levels in the ARC. Administration of oPRL to pup-deprived dams increased preproenkephalin mRNA levels in the arcuate and ventromedial nuclei and reduced POMC mRNA levels in the ARC to levels similar to suckled control levels. In conclusion, POMC neurons in the ARC appear to be refractory to PRL regulation in the presence of a suckling stimulus, and other components of the suckling stimulus may buy parlodel contribute to the suppression of POMC mRNA levels during lactation. By contrast, PRL provides a regulatory influence for the suckling-induced increase in preproenkephalin mRNA signal levels in arcuate and ventromedial nuclei.

parlodel dosage used 2015-11-07

The term gigantomastia has been used buy parlodel to describe breast enlargement to extreme size, with sloughing, haemorrhage and infection. The condition is rare and a case of pregnancy-related gigantomastia is reported.

parlodel alcohol 2016-11-01

Restoration of buy parlodel prolactin levels with bromocriptine.

bromocriptine parlodel dosage 2017-02-14

SKF82958 alone significantly increased PKA-mediated phosphorylation of both DARPP-32 and NR1. Bromocriptine alone had no effect on pDARPP-32 or on pNR1. However, when D1 receptors were blocked, bromocriptine reduced the PKA-mediated phosphorylation of both DARPP-32 and NR1. Coincident treatment with bromocriptine and ethanol reversed both of these buy parlodel effects with D1 receptors blocked. The combination of eticlopride (D2 blocker) and SF82958 (D1 agonist) did not significantly alter either pDARPP-32 or pNR1.

buy parlodel online 2015-09-26

Effects of hyperthermia alone and combined with bromocriptine (BC) or a somatostatin analogue (SMS 201-995) were studied in vitro on normal pituitary and pituitary tumour cells (GH3 cells). GH3 cells were more sensitive to heat than normal pituitary cells and a Zovirax Suspension maximal difference in survival was obtained with hyperthermia at 42.5 degrees C for 6 h. BC had cytotoxic and antiproliferative effects on GH3 cells, whereas SMS 201-995 was not effective. Hyperthermia at 42.5 degrees C for 3 h in combination with BC enhanced selective cytotoxicity for GH3 cells. In contrast, combined treatment with hyperthermia and SMS 201-995 failed to enhance cytotoxicity for GH3 cells. The combination of hyperthermia and BC could provide improved therapeutic efficacy in patients with pituitary adenomas.

parlodel tablet uses 2017-10-06

The specific binding of [3H]spiperone (35 pM), as defined by the D-2 antagonist sulpiride, was potently displaced by ergot derivatives of both the ergoline and ergopeptine type, and by dopamine agonists and antagonists. The potency of the ergot derivatives ranged widely from an IC50 value of 3 nM Levitra Sales Online for bromocriptine to a value of 1000 nM for the partial ergoline, LY-141865. GTP and its stable analogue, guanyl-5'-yl-imidodiphosphate (Gpp(NH)p), did not affect the affinity (100 pM) or density (30 pmol/g wet wt) of [3H]spiperone binding sites, but did decrease the potency of a number of ergoline compounds including pergolide, lergotrile and LY-141865, as well as dopamine agonists to displace [3H]spiperone binding. The affinities of the ergopeptines, bromocriptine and dihydroergocryptine, and of the isolysergic acid ergoline, lisuride, and dopamine antagonists were unaltered by the presence of guanine nucleotides. The effect was specific for guanine nucleotides, with near maximal effects on agonist affinity observed in the presence of a 100 microM concentration of nucleotide. The relative decrease in affinity found in the presence of GTP or Gpp(NH)p varied widely for individual ergot derivatives and dopamine agonists. The largest decrease was seen with dopamine itself, and agonists such as the tetralins and with LY-141865. Many ergolines had shifts in potency between those seen for agonists and antagonists, suggesting a partial agonist action at D-2 receptors. Guanine nucleotide sensitivity may represent a valuable in vitro method for studying the agonist/antagonist properties of dopaminergic drugs, such as the semi-synthetic ergoline compounds.

parlodel drug class 2016-08-05

We report a patient with a previously known primary antiphospholipid syndrome who had life threatening multiple arterial thromboses. The patient experienced a myocardial infarction with intraventricular thrombi under bromocriptine therapy in the puerperium, despite prophylactic low molecular weight heparin therapy. In this patient, no microvascular involvement was identified, thus eliminating the diagnosis of catastrophic antiphospholipid syndrome. Arterial thromboses may be explained by peripheral emboli originating from the intraventricular thrombi. This case emphasizes the necessity of a careful evaluation of the risk-benefit balance of bromocriptine therapy Aldactone Acne Reviews in patients with arterial risk factors. It also emphasizes the need for a correct diagnosis of catastrophic antiphospholipid syndrome allowing to limit the prescription of aggressive therapies.

parlodel 30 mg 2015-01-01

The possible mutagenic and DNA-synthesis inhibitory effects of 2-bromo-alpha-ergocryptine, a new semi-synthetic ergot alkaloid, was studied in human and rabbit lymphocytes exposed to it in vivo and in vitro. The analysis of SCE was mainly used to evaluate potential mutagenicity, and the mitotic and DNA-synthesis inhibition was explored by examining the proportions of first-, second- and third-division metaphases in the corresponding lymphocyte cultures. The results obtained show that 2-bromo-alpha-ergocryptine does not induce SCE in the cell systems tested, or structural chromosome aberrations in human lymphocytes in vivo. On the other hand, a marked Effexor Sa Dosing mitotic inhibitory effect and associated cell kinetic changes could be clearly attributed to the drug, probably related to its cytotoxicity.

parlodel medication 2015-09-19

1. Measurements of arteriovenous differences across mammary glands of normal and starved lactating rats, and lactating rats made short-term insulin-deficient with streptozotocin or prolactin-deficient with bromocryptine, showed that only Coreg 10 Mg in the starved animals was there a significant decrease in glucose uptake. This decrease was accompanied by release of lactate and pyruvate from the gland, in contrast with the uptake of these metabolites by glands of normal lactating rats. 2. There were no marked differences in metabolite concentrations in freeze-clamped glands in the four conditions studied, apart from a decrease in [lactate] and [pyruvate] and an increase in [glucose] in the glands of the streptozotocin-treated group. 3. Acini isolated from the glands of starved, insulin or prolactin-deficient rats had a higher production of lactate and pyruvate from glucose than did glands from normal rats; this is in agreement with the reported decrease in the proportion of active pyruvate dehydrogenase in these situations [Field & Coore (1976) Biochem. J.156, 333-337; Kankel & Reinauer (1976) Diabetologia12, 149-154]. 4. Addition of insulin did not increase the uptake of glucose by acini from normal glands, but it caused a significant increase in the utilization of glucose by acini from glands of starved rats. Insulin did not decrease the accumulation of lactate and pyruvate in any of the experiments. 5. It is concluded that isolated acini represent a suitable model for the study of mammary-gland carbohydrate metabolism in that they reflect metabolism of the gland in vivo.

parlodel drug classification 2017-07-27

Two multigravida patients with no prior psychiatric history were seen with postpartum psychosis, having received bromocriptine for inhibition of lactation. Bromocriptine given in high doses Benicar Generic Launch has been associated with psychosis in patients receiving the drug for Parkinson's disease. These cases demonstrate that bromocriptine may cause psychosis even when given in low doses.

parlodel dosing 2016-05-31

Three ergot derivatives, lisuride, lergotrile and bromocriptine, given to rats trained to eat 4 h a day, induced a dose- and time-related anorexia. They were more potent in this context than either amphetamine or fenfluramine. Lisuride and lergotrile failed to increase locomotor activity or to induce stereotyped behaviour at doses corresponding to the ID50 on food intake. At this dose, bromocriptine slightly stimulated motor activity. The anorectic effect of the three compounds was selectively antagonized by blockers of dopamine ( Duphaston Medicine Usage DA) receptors in the central nervous system but not by either inhibiton of catecholamine synthesis or blockade of alpha- or beta-adrenoceptors or of serotonergic receptors. Also two blockers of 'peripheral' DA receptors failed to antagonize ergoline-induced anorexia. These findings indicate that stimulation of DA receptors involved in feeding behaviour was responsible for the anorexigenic effect of the ergot derivatives investigated. In most instances this effect occurred at dose levels which failed to induce central stimulant effects.

parlodel medicine 2016-10-20

All three patients' presentations were Atarax Dosage Pediatrics initially unremarkable, but later each had persistent and relentlessly increasing serum prolactin concentrations and evidence of distant spread of their tumours. The first patient presented aged 32 and was treated with repeated transsphenoidal resections of the tumour, pituitary radiotherapy, high dose bromocriptine therapy, the somatostatin analogue octreotide and chemotherapy. Nine years after the original diagnosis a liver biopsy revealed carcinoma cells positively immunostaining for prolactin. At autopsy further microscopically similar metastases were seen in both lungs and the left hilar lymph nodes. The second patient presented aged 48 and was treated with external beam pituitary radiotherapy, bromocriptine, transsphenoidal hypophysectomy and chemotherapy. Fifteen years after the original diagnosis bone biopsy revealed carcinoma cells positively immunostaining for prolactin; the patient developed interstitial nephritis and died in renal failure. The third patient presented aged 48 with hypogonadism and bitemporal hemianopia due to a macroadenoma. This was removed transfrontally and followed by external beam radiotherapy. After recurrence, further surgery and radiotherapy were undertaken, but the tumour continued to grow and the patient died suddenly of a pulmonary embolus. At autopsy, tumour was found in thoracic lymph nodes and lung capillaries.