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Persantine (Dipyridamole)

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Generic Persantine is a coumarin anticoagulants. Generic Persantine is indicated as an adjunct to coumarin anticoagulants in the prevention of postoperative thromboembolic complications of cardiac valve replacement. Generic Persantine keeps blood flowing smoothly by preventing blood cells from clumping together (coagulating).

Other names for this medication:

Similar Products:
Argatroban, Plavix, Salagen, Arixtra


Also known as:  Dipyridamole.


Generic Persantine is a coumarin anticoagulants.

Generic Persantine is indicated as an adjunct to coumarin anticoagulants in the prevention of postoperative thromboembolic complications of cardiac valve replacement. Generic Persantine keeps blood flowing smoothly by preventing blood cells from clumping together (coagulating).

Persantine is also known as Dipyridamole.

Generic name of Generic Persantine is Dipyridamole.

Brand name of Generic Persantine is Persantine.


You can take Generic Persantine with or without food.

The recommended Generic Persantine dose is 75-100 mg four times daily.

Try to take this Generic Persantine at the same time each day.

Do not store in the bathroom.

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


If you overdose Generic Persantine and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Persantine overdosage: warm feeling, flushes, sweating, restlessness, weakness, dizziness.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. 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 Persantine 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.


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

Be careful with Generic Persantine if you are pregnant, planning to become pregnant, or are breast-feeding.

Be careful with Generic Persantine if you have unstable angina.

Be careful with Generic Persantine if you have had recently sustained myocardial infarction or hypotension.

Be careful with Generic Persantine if you use anticoagulants ("blood thinners"), aspirin, valproic acid.

It can be dangerous to stop Generic Persantine taking suddenly.

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The stenosis decreased posterior wall thickening to 50% of control, and posterior subendocardial blood flow from 1.48(0.27) to 0.61(0.19) ml.min-1.g-1 in group I and from 1.49(0.23) to 0.62(0.18) ml.min-1.g-1 in group II. Subendocardial blood flow was further decreased after administration of either nisoldipine [0.37(0.20) ml.min-1.g-1, p < 0.05 v stenosis] or dipyridamole [0.22(0.11) ml.min-1.g-1, p < 0.05 v stenosis]. Regional myocardial blood flow in the anterior region was increased. The drug induced reduction of subendocardial blood flow decreased posterior wall thickening further from 9.3(2.1) to 6.2(3.9)% (p < 0.05 v stenosis, group I) and from 9.1(1.7) to 4.3(2.4)% (p < 0.05 v stenosis, group II). When the drug induced decrease in aortic pressure was reversed, subendocardial blood flow again increased in group I [0.63(0.19) ml.min-1.g-1, p < 0.05 v stenosis and nisoldipine] whereas in group II it remained decreased [0.40(0.29) ml.min-1.g-1, NS v stenosis and dipyridamole]. There was restoration of posterior wall thickening in group I [10.4(3.8)%, p < 0.05 v stenosis and nisoldipine], but not in group II [5.2(3.5)%, NS v stenosis and dipyridamole].

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In order to follow the filtration of a red cell suspension with time, the filtration technique described (1) has been modified. The red cell suspension is filtered through a polycarbonate membrane filter (pore diameter 5 micron) under gravitational force. The filtrate is collected in a plastic tube connected to an isometric transducer, the output of which is registered on a chart recorder. The linear part of the curve obtained is used to calculate the slope and the relative filterability (RF) ie the ratio of the rate of flow of the red cell suspension to the rate of flow of the suspending medium. The reproducibility of the technique is demonstrated by a less than 5% coefficient of variation in one blood sample less than 5% interobserver variation and a weekly variation from the same donor of less than 5%. The fast filtration rate of a highly diluted red cell suspension (0.5-1%) may be followed with this technique, taking the first 15 seconds to calculate it. The technique has proved useful in detecting differences in red cell deformability in connective tissue disorders (Scleroderma, Raynaud's phenomenon) also between stored and freshly prepared red cell suspension and its improvement by drugs (pentoxifylline, dipyridamole).

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Dipyridamole echocardiography, dobutamine-atropine echocardiography, exercise stress testing, and coronary angiography.

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The study considered a consecutive series of patients with significant CA (stenosis > or = 50%), studied with echo-B mode and Doppler velocity scans chosen from all patients in the diagnostic vascular cerebral laboratory, between May 1992 and January 1994, for a non invasive study of neck arteries. The protocol of the multidisciplinary study included: history of risk factors (RF); neurologic evaluation; peripheral vascular evaluation with Doppler velocity scans; cardiac evaluation, and patients without clinical history of MI underwent a maximal stress test (ST). If there was bilateral carotid occlusion or non-evaluated ST the patients underwent echo-stress with dipyridamole (ED) or myocardial scintigraphy stress test (MS); haematologic tests, CT in patients with symptoms of cerebral ischemia; arteriography of epi-aortic arteries in patients with indication for carotid enderterectomy.

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In a 4-year period, 84 patients who were referred for a dipyridamole thallium-201 stress test to rule out significant coronary artery disease had normal scans. A dipyridamole study was recommended instead of exercise because of arthritis, severe obesity, peripheral vascular disease, pulmonary disease, other chronic illnesses, or combinations of these problems. All patients had three-view (i.e., anterior, shallow left anterior oblique, and steep left anterior oblique) planar thallium-201 imaging 10 minutes and 3.5 hours after administration of 0.6 mg/kg of intravenous dipyridamole. The patients were followed for 42 +/- 13 (range 1-58) months to document the cardiac event rate. Of the 84 patients with normal results, 14 died during the follow-up period from noncardiac causes. Three other patients died 29-51 months after the test due to an acute myocardial infarction, a probable acute myocardial infarction, and sudden cardiac death, respectively. Of the survivors, 5 suffered an acute myocardial infarction 28-50 months after the dipyridamole thallium scan and 1 had coronary artery bypass grafting due to increasing angina pectoris 58 months after the scan (overall cardiac event rate of 0.4% per year). Of the remaining 61 patients, 39 (64%) were asymptomatic, 20 (33%) had the same symptoms they had at the time of testing without significant deterioration, while 2 patients (3%) had deterioration of their chest pains but no cardiac complication. Thus, in this group of patients, a normal dipyridamole thallium-201 perfusion scan predicted a good cardiovascular outcome for at least 24 months following the test.

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The mean age of patients with coronary artery thrombosis (5 males and 1 female) was (17.2 ± 11.3) months.Five cases had thrombosis in left coronary artery (LCA), and four cases had thrombosis in aneurysm of left anterior descending artery (LAD). One case had thrombosis in both left and right coronary artery (RCA).One case died. Maximum thrombus was about 1.60 cm × 0.80 cm, locating in LAD. The diameter of LCA and RCA was (0.44 ± 0.07) cm and (0.45 ± 0.07) cm. Two patients showed abnormal ECG. Case 3 showed ST segment depression in lead V5. Case 6 showed myocardial infarction.In acute phase of KD, three patients received treatment with intravenous immunoglobin (IVIG), five patients were treated with aspirin.In sub-acute and convalescent phase of KD, all patients were treated with low-dose aspirin.Warfarin and dipyridamole were applied in 5 patients. All cases were treated with thrombolytic therapy using urokinase and/or heparin. After thrombolytic therapy, echocardiography showed thrombolysis in four cases and no change in one.One patient died of myocardial infarction.

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In this study, we have investigated the mechanism of ADP-induced relaxation of porcine coronary artery (PCA) rings. The P2Y receptor agonists ADP and ADPbetaS produced concentration-dependent relaxation of endothelium-denuded PCA smooth muscle with pD2 values of 5.3 and 4.9, respectively. RT-polymerase chain reaction (RT-PCR) and immunoblotting demonstrated mRNA and protein expression of P2Y1 and A2A adenosine receptors in the PCA. The nonselective P2 antagonist PPADS or the P2Y1-selective antagonist MRS2179 failed to alter ADP- or ADPbetaS-induced relaxations. Relaxations to ADP were, however, blocked by the A2A adenosine receptor-selective antagonists ZM241385 and SCH58261 (apparent pK(B) values of 9.2 and 8.9, respectively). We excluded roles for direct occupancy of A2A adenosine receptors by ADP or ADPbetaS as well as metabolism to adenosine as mechanisms for ADP-evoked relaxations. However, ADP responses were significantly enhanced in the presence of the ENT1 nucleoside transporter inhibitors dipyridamole and NBTI and were significantly inhibited by adenosine deaminase, indicating a role for extracellular adenosine. Suprafusion of [3H]-adenine-labeled PCA segments showed that ADP induced the release of a number of purines, including adenosine. These data suggest that ADP mediates relaxation of the PCA via a novel mechanism that involves adenine nucleotide-evoked adenosine release and the subsequent activation of A2A receptors.

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To review the methods used for preoperative cardiac risk stratification of patients having peripheral vascular surgery.

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The aim of this study was to evaluate the diagnostic potential of low-dose adenosine stress echocardiography in detection of myocardial viability.

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Apolipoprotein A-IV (apoA-IV) might play an important role in lipoprotein metabolism, including modulation of triglyceride-rich lipoprotein catabolism, reverse cholesterol transport and cholesteryl ester transfer protein (CETP) activity. Increased apoA-IV levels have been reported in plasma from NIDDM patients. The aim of the present study was to look for a possible association between plasma apoA-IV level and prevalence of macrovascular disease in NIDDM. One hundred and thirty-six NIDDM patients were studied (71 men, 65 women). Macrovascular disease was assessed in each patient by a standardized questionnaire, physical examination, resting electrocardiogram (ECG), and laboratory evaluation (ankle/arm blood pressure ratio, continuous wave Doppler velocimetry). Moreover, patients without any history of coronary heart disease and showing a normal resting ECG underwent a bicycle exercise test or a dipyridamole thallium scintigraphy to detect possible silent myocardial ischemia. Among the 136 NIDDM patients, 56 had macrovascular disease. ApoA-IV levels were significantly higher in NIDDM patients with macrovascular disease than in NIDDM patients without macrovascular disease (20.9 +/- 8.6 vs. 13.3 +/- 5.3 mg/dl; P < 0.001). The influence of different factors, such as age, BMI, cigarette smoking, hypertension, total cholesterol, triglycerides, HDL cholesterol, apoA-IV level, apoA-IV phenotype, fasting glycemia, fasting C-peptide, and microalbuminuria, on the prevalence of macrovascular disease was analyzed using a logistic regression model. In the univariate analysis, apoA-IV level (P < 0.00001), age (P = 0.0087), hypertension (P = 0.012), microalbuminuria (P = 0.018), triglycerides (P = 0.02), and fasting C-peptide (P = 0.03) were positively associated with macrovascular disease. In the multivariate analysis, macrovascular disease was positively associated only with apoA-IV (P < 0.0001) and age (P = 0.003) and negatively associated with HDL cholesterol (P = 0.013). These results indicate that increased plasma apoA-IV level is associated with an increased prevalence of macrovascular disease in NIDDM. Moreover, apoA-IV, in NIDDM patients, appears to be a better marker for macrovascular disease than triglycerides.

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Throughout the central nervous system extracellular adenosine serves important neuroprotective and neuromodulatory functions. However, current understanding of the in vivo regulation and effects of adenosine is limited by the spatial and temporal resolution of available measurement techniques. Here, we describe an enzyme-linked microelectrode array (MEA) with high spatial (7500 µm(2)) and temporal (4 Hz) resolution that can selectively measure extracellular adenosine through the use of self-referenced coating scheme that accounts for interfering substances and the enzymatic breakdown products of adenosine. In vitro, the MEAs selectively measured adenosine in a linear fashion (r(2)=0.98±0.01, concentration range=0-15 µM, limit of detection =0.96±0.5 µM). In vivo the limit of detection was 0.04±0.02 µM, which permitted real-time monitoring of the basal extracellular concentration in rat cerebral cortex (4.3±1.5 µM). Local cortical injection of adenosine through a micropipette produced dose-dependent transient increases in the measured extracellular concentration (200 nL: 6.8±1.8 µM; 400 nL: 19.4±5.3 µM) [P<0.001]. Lastly, local injection of dipyridamole, which inhibits transport of adenosine through equilibrative nucleoside transporter, raised the measured extracellular concentration of adenosine by 120% (5.6→12.3 µM) [P<0.001]. These studies demonstrate that MEAs can selectively measure adenosine on temporal and spatial scales relevant to adenosine signaling and regulation in normal and pathologic states.

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To test the hypothesis that anti-platelet aggregation therapy administered to the elderly patients may be helpful in preventing pressure ulcer formation, the medical records of 132 bedridden elderly patients were analyzed. In addition, the propensity of platelets to aggregate was also measured in some of the bedridden patients.

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To study the growth inhibitory and apoptotic effects of adenosine triphosphate (ATP) and adenosine (ADO) on human gastric carcinoma (HGC)-27 cells in vitro and the mechanisms related to the actions of ATP and ADO.

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Adenosine exerts anti-aggregatory effects on human platelets in vitro, probably by increasing intraplatelet levels of cyclic AMP. In addition, adenosine prevents platelet loss in vivo. We have studied the relationship between the concentration of adenosine in the platelet media and the level of cAMP. In PRP, exogenous adenosine (2-16 microM) was eliminated with a half-life close to 5 min. Approximately half of the added adenosine was deaminated (blocked by 1-2 microM EHNA), and half was eliminated by uptake into platelets (blocked by 2 microM dipyridamole). In whole blood the half-life for adenosine was much shorter, about 15 s. Addition of adenosine deaminase (0.3 microgram ml-1) to PRP resulted in a measured half-life for adenosine approximating that of whole blood. In PRP where adenosine was eliminated as quickly as in whole blood, the adenosine-mediated stimulation of cAMP was 35% lower than in PRP, and the cAMP response lasted 2 min versus 15 min in normal PRP. These results suggest that the magnitude and duration of adenosine's effect on platelets are markedly overestimated by studying platelet suspensions. In blood, the effect of adenosine is smaller in magnitude and very transient. The possibility is discussed that the action of adenosine in vivo on blood platelets can therefore be quite local.

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Thirty-five patients with end-stage coronary artery disease and class III (Canadian Cardiovascular Society) angina were included. Myocardial ischemia was evaluated with dipyridamole PET scanning and exercise tolerance with bicycle ergometry. Ten patients were treated with naked plasmid DNA encoding for human VEGF165 (VEGF) and 12 patients were treated with laser therapy (direct myocardial revascularization [DMR]) using an electromechanical mapping system. Thirteen patients were treated with standard medical therapy (control).

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A uniform protocol for thallium scintigraphy of the myocardium has been issued in Austria to avoid difficulties in interpreting results and to avoid repeated examinations to save expenses and radiation burden. From the beginning of 1995 this protocol will be used in the Austrian departments of Nuclear Medicine, differences from this protocol have to be mentioned separately. In this protocol the procedure of examination, bicycle and pharmacological stress testing and vasodilatation, acquisition techniques for planar and SPECT imaging, data processing and quality control of devices are defined.

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We investigated the antinephritic effects of TJ-8014, in comparison to dipyridamole, on crescentic-type anti-GBM nephritis in rats. When administration of test drugs was started from the heterologous phase (from the day after the anti-GBM serum injection), TJ-8014 at 2.0 g/kg/day, p.o., markedly inhibited the urinary protein excretion and elevations of plasma cholesterol and urea nitrogen levels as well as glomerular histopathological changes (i.e., crescent formation, adhesion and fibrinoid necrosis) throughout the 40-day observation period. TJ-8014 at 0.1 and 0.5 g/kg/day, p.o., and dipyridamole at 0.4 g/day, p.o., inhibited only the histopathological changes. When treatment was started from the autologous phase (from the 22nd day after the anti-GBM serum injection) after the disease had been established, only the high dose of 5.0 g/kg/day of TJ-8014, p.o., was effective in improving the histopathological changes of the established nephritis, as assessed on the 53rd day. The low doses of TJ-8014 and dipyridamole were ineffective. These results suggest that TJ-8014 may be a useful Japanese herbal medicine against rapidly progressive glomerulonephritis, which is characterized by severe glomerular lesions with the extensive formation of crescents. Furthermore, the mechanisms of action of this medicine will be discussed.

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The safety of ergonovine/ergometrine stress testing for coronary vasospasm when performed outside the cardiac catheterization laboratory (cath lab) has been questioned vigorously.

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Baseline echocardiography showed wall motion abnormalities in 9 patients (excluded from donation). Stress echocardiography was performed in the remaining 13 patients. Results were normal in 8, who were uneventfully transplanted in marginal recipients. Stress results were abnormal in 5 (excluded from donation). STE was obtained in all cases (100% feasibility) and ΔGLS was significantly different between normal and pathological stress-echo (+13.2 ± 5.2 versus -6.1% ± 3.1%, P = .0001, respectively).

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Adenosine is a potent vasodilator used clinically in nuclear scintigraphy to assess coronary artery reserves. The potential to identify this vasodilating effect of adenosine using magnetic resonance imaging (MRI), which is superior in spatial resolution to nuclear scintigraphy, combined with a blood-pool MRI contrast agent, was investigated in normal rats.

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Sixty-seven patients (52 male, mean age 52+/-12 years) with different degrees of idiopathic LV systolic dysfunction (average LV ejection fraction, 0.34+/-0.10; range, 0.07 to 0.49) were prospectively enrolled. Thirty-four subjects (51%) had no history of heart failure symptoms at enrollment (NYHA class I). All patients underwent clinical and functional evaluation and a PET study to measure absolute MBF at rest and after intravenous dipyridamole. During a mean follow-up of 45+/-37 months, 24 patients had major cardiac events, including cardiac death in 8 and development or progression of heart failure in 16 patients. Multivariate regression analysis (Cox proportional hazards model) revealed heart rate (chi(2) 11.06, P<0.001), LV end-diastolic dimension (chi(2) 11.73, P<0.001), and dipyridamole MBF (chi(2) 11.04, P<0.001) as independent predictors of subsequent cardiac events. Dipyridamole MBF < or = 1.36 mL. min(-1). g(-1) was associated with an increase in the relative risk of death, development, or progression of heart failure of 3.5 times over other more common clinical and functional variables.

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End-stage renal disease (ESRD) patients often require either the formation of an arteriovenous (AV) fistula or an AV interposition prosthetic shunt for haemodialysis. These access sites should ideally have a long life and a low rate of complications (for example thrombosis, infection, stenosis, aneurysm formation and distal limb ischaemia). Although some of the complications may be unavoidable, any adjuvant technique or medical treatment aimed at decreasing complications would be welcome. This is the second update of the review first published in 2004.

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Tariquidar, MK571, frusemide and dipyridamole all significantly increased the intracellular accumulation of lopinavir in the PBMCs, whereas probenecid decreased it. The cellular accumulation ratio (CAR) of lopinavir was also increased by ritonavir, amprenavir and atazanavir in a concentration-dependent manner in both cell types. The expression of P-gp, MRP1 and MRP2 mRNA were variable and individually did not correlate with CARs of lopinavir.

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There is limited evidence suggesting that restenosis/reocclusion at six months following peripheral endovascular treatment is reduced by use of antiplatelet drugs compared with placebo/control, but associated information on bleeding and gastrointestinal side effects is lacking. There is also some evidence of variation in effect according to different drugs with cilostazol reducing reocclusion/restenosis at 12 months compared with ticlopidine and both LMWH and batroxobin combined with aspirin appearing beneficial compared with aspirin alone. However, available trials are generally small and of variable quality and side effects of drugs are not consistently addressed. Further good quality, large-scale RCTs, stratified by severity of disease, are required.

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The objective of the present studies was to examine adenosine uptake in the rat luteal cell, to characterize the cellular products after uptake, and to assess the role of adenosine transport and conversion to cAMP in amplification of LH-stimulated cAMP accumulation. Adenosine uptake showed an apparent Km of 7.3 +/- 0.6 microM, and a maximum velocity of 2.2 +/- 1.4 pmol/min X 10(5) cells at 24 C; uptake was temperature dependent (Q10 = approximately 3) and inhibited by dipyridamole (IC50 = 7 microM). Radiolabeled adenosine uptake was inhibited by AMP (IC50 = 14 microM), ATP (IC50 = 16 microM), guanosine (IC50 = 20 microM), inosine (IC50 = 22 microM), ADP (IC50 = 26 microM), and theophylline (IC50 = 5 mM); no inhibition by adenine, hypoxanthine, xanthine, prostaglandin F2 alpha (PGF2 alpha), PGE2, or LH was seen. Cellular products of radiolabeled adenosine uptake were found primarily in the trichloroacetic acid-soluble fraction (88%), and 90% of the radioactivity in this fraction comigrated with adenine nucleotides on electrophoresis; time-dependent incorporation of radioactivity into RNA, DNA, and protein was also seen. Adenosine transport did not appear to be related to the functional state of the luteal cell; for example, no change in the characteristics of uptake was seen in cells obtained from hypophysectomized animals or in cells incubated directly with PGF2 alpha or LH. Adenosine increased cell ATP levels in a dose-dependent manner in parallel with amplification of LH-stimulated cAMP accumulation. A substantial proportion of the total cAMP produced by the cells was derived from extracellular adenosine (40-90%). This response was directly related to the concentration of adenosine, and LH increased the magnitude of cAMP derived from adenosine by about 2-fold. Based on the present studies, adenosine uptake in the luteal cell appears to occur by a dipyridamole-sensitive, phosphorylation-dependent transport system which is independent of pituitary hormones or PG regulation. Moreover, amplification of LH-dependent cAMP accumulation by adenosine appears to be primarily a mass effect due chiefly to utilization of extracellular adenosine by the cell as a prosubstrate for conversion into cAMP by adenylate cyclase.

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Adenosine inhibits proliferation of cardiac fibroblasts and hypertrophy of cardiomyocytes, both of which may play crucial roles in cardiac remodeling. In the present study, we investigated whether chronic stimulation of adenosine receptors begun after myocardial infarction (MI) prevents cardiac remodeling.

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Patients in sinus rhythm with stable CAD were enrolled in this prospective, randomized, double-blind trial. Patients had to be in a stable condition for at least 15 days before enrollment, on their usual therapy. Patients who were receiving beta-blockers or ivabradine entered a 2-week washout period from these drugs before randomization. Transthoracic Doppler-derived CFVR was assessed in left anterior descending coronary artery, and was calculated as the ratio of hyperemic to baseline diastolic coronary flow velocity (CFV). Hyperemic CFV was obtained using dipyridamole administration using standard protocols. After CFVR assessment, patients were randomized to ivabradine or bisoprolol and entered an up-titration phase, and CFVR was assessed again 1 month after the end of the up-titration phase.

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Increased lung uptake of thallium has less ominous short term prognostic significance when observed in association with dipyridamole stress rather than with exercise.

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In patients with chronic stable angina treated with regular antianginal background medication, the use of oral dipyridamole is safe and well tolerated. Antianginal and antiischaemic efficacy, as assessed by exercise testing, is comparable to placebo, except for a beneficial effect on time to ischaemia after 2 months, totally attributable to patients with lower exercise tolerance at study entry.

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persantine medication 2015-03-04

The authors have previously reported that dipyridamole decreased platelet-derived growth factor levels in human serum by lowering the release of this factor during blood clotting. In the present study, we have shown that this effect is specific to buy persantine dipyridamole, and does not occur with other antiplatelet drugs such as aspirin, trapidil or ticlopidine. In addition, dipyridamole has been shown to decrease the PDGF level selectively, but not the levels of other factors from alpha granules in platelets (beta-thromboglobulin and platelet factor 4). These data indicate that dipyridamole may be an effective drug for the prevention of PDGF-related disorders.

persantine drug classification 2016-01-15

The present study analyzed coronary sinus blood flow alterations after dipyridamole induced coronary vasodilation in seven patients whose endomyocardial biopsies evidenced no sign of rejection (group 1) and in five patients with histologic signs of rejection (group 2) after orthotopic heart transplantation. All patients were treated with cyclosporine and prednisone and some with azathioprine and had normal coronary arteriograms. Coronary sinus blood flow and coronary resistance were measured before and after intravenous dipyridamole (0.18 mg/kg/min over 4 minutes). Basal values were similar in groups 1 and 2 for coronary sinus blood flow (166 +/- 34 compared with 181 +/- 39 ml/min, respectively), coronary resistance (0.62 +/- 10 compared with 0.52 +/- 13 mm Hg/ml/min, respectively), coronary sinus blood oxygen content (5.7 +/- 1.6 compared with 4.5 +/- 0.9 ml/100 ml, respectively) and arterial-coronary sinus buy persantine blood oxygen difference (10.6 +/- 1.3 compared with 10.3 +/- 1.8 ml/100 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

persantine oral dose 2016-02-05

We evaluated the interaction of several nucleoside transport inhibitors and substrates with the binding of [3H]nitrobenzylthioinosine ([3H]NBMPR) to nucleoside transport sites in guinea pig cardiac sections. Using quantitative autoradiography, we determined inhibition constants for inhibition of [3H]NBMPR binding to both coronary endothelial cells and cardiac myocytes. We studied the interactions of NBMPR, nitrobenzylthioguanosine, dipyridamole, dilazep, hexobendine, lidoflazine, mioflazine, soluflazine, adenosine, inosine and uridine for these two cell types. Of buy persantine the compounds tested in this study, lidoflazine (8.2X) and hexobendine (6.3X) have the greatest selectivity for coronary endothelial cell nucleoside transporters. All other compounds had 3-fold or less selectivity. Therefore, there is evidence of nucleoside transporter subtypes between endothelial cells and myocytes. This heterogeneity of transport inhibitory sites on nucleoside transporters may allow the development of agents to modulate selectively some of the cardiovascular effects of adenosine.

persantine dosage chart 2015-07-18

We recently demonstrated in isolated, perfused hearts that radiolabeled pyruvaldehyde bis(N4-methylthiosemicarbazonato)copper(II) (Cu-PTSM) is well extracted throughout a range of conditions including ischemia, hypoxia, and hyperemia. Once extracted, buy persantine binding of radioactivity by the isolated heart was essentially irreversible, giving this tracer microspherelike qualities. Because Cu-PTSM can be readily prepared with the generator-produced positron-emitting copper 62 and other gamma- or positron-emitting copper radionuclides, we evaluated its usefulness for measuring regional myocardial and renal blood flow in vivo in intact dogs at rest, after ischemia, or after coronary hyperemia was induced by intravenous administration of dipyridamole. After intravenous administration of radiolabeled Cu-PTSM, the tracer cleared rapidly from the blood. Myocardial uptake of single photon-emitting 67Cu-labeled Cu-PTSM was measured directly in myocardial samples 15 minutes after tracer administration, and it increased proportionally with blood flow throughout the flow range (estimated concomitantly with radiolabeled microspheres) of 0.0-6.0 ml/g/min (n = 340 samples from 17 dogs, r = 0.99, Ycopper radioactivity = 85Xmicrosphere flow -7 chi 2 + 17). Renal uptake of radiolabeled Cu-PTSM was also proportional to blood flow. Positron emission tomography was performed in four intact dogs after intravenous administration of 64Cu-labeled Cu-PTSM (19% positron decay, t1/2 = 12.8 hours). High-quality images of heart and kidney were obtained. Accordingly, radiolabeled Cu-PTSM should be a useful, generator-produced tracer for estimating regional myocardial and renal blood flow with positron emission tomography.

persantine drug 2016-01-27

Proceeding directly to vascular surgery resulted in the poorest 5-year survival rate (77.4%) compared with preoperative risk stratification followed by selective coronary revascularization, routine noninvasive testing (86.1%), selective testing (86.0%), and routine angiography (87.9%; p = 0.00). The incremental cost-effectiveness ratio for selective testing buy persantine was significantly lower than for routine angiography ($44,800/years of life saved (YLS) v $93,300/YLS; p < 0.02). Routine noninvasive testing was not cost-effective. Thirty-day mortality was the same for all four strategies (p = 0.84).

persantine overdose 2017-02-07

Landmark clinical trials and other studies pertaining to buy persantine atherothrombosis in women (including risk factors, clinical outcomes, and treatment patterns) were obtained through Pubmed and Medline literature research and reviewed.

persantine brand name 2016-11-21

A routine secondary pharmacology screen indicated that reversibly binding oral P2Y(12) receptor antagonist ticagrelor could buy persantine inhibit adenosine uptake in human erythrocytes, suggesting that ticagrelor may potentiate adenosine-mediated responses in vivo. The aim of this study was to further characterize the adenosine uptake inhibition in vitro and study possible physiological consequences of adenosine uptake inhibition by ticagrelor in an anesthetized dog model of coronary blood flow compared to dipyridamole.

persantine dosage 2015-01-22

We report the clinical, echocardiographic and therapeutic aspects and the evolution of 7 cases of right cardiac migrant thromboembolus in pulmonary embolism (5 M and 2 F, aged 43 to 91). Our data are also compared with all the buy persantine cases reported in the literature (77 patients). During a sample year (1987) we systematically performed two-dimensional echocardiograms (2D Echo) as early as possible in all the patients admitted to our Coronary Care Unit for suspected pulmonary embolism; among 42 patients the diagnosis of pulmonary embolism was confirmed in 30 out of 42 patients. A relatively high incidence of thromboembolus was found (5/30, 17% in 1987); this finding seems to be relative to the early execution of the 2D Echo study (thromboembolus was found in 4/5 patients when 2D Echo was performed within 20 hours and in only 1/23 when 2D Echo was performed later). The 2D Echo was always evocative of freely floating migrant thromboembolus (6 in right atrium, 1 in right ventricle) and no differential diagnosis with thrombi in situ or other masses was necessary. The therapy for 6 patients hospitalized for pulmonary embolism and surviving the first hours (1 patient died immediately) was: surgical in 1 case, medical in the other 5. Medical therapy consisted only of heparin-calcium in one patient and heparin-calcium + dipyridamole in another because of contra-indications for more aggressive therapy. One patient underwent anticoagulant therapy with i.v. heparin. The remaining two underwent fibrinolytic therapy with urokinase and, afterwards, anticoagulant therapy: in 1 case the therapy was started after the embolization of the mass in the pulmonary artery had occurred; in the other one we observed the progressive reduction of thromboembolus until its disappearance within 5 days without any signs of further embolization. All patients survived and were discharged within 25 days, despite the occurrence of lung embolization in 4 of them. The review of 77 cases reported in the literature shows good outcomes for embolectomy when compared with medical therapy, but almost half of the patients underwent surgical therapy directly. Medical therapy experience, particularly with thrombolytic agents (10 cases in all), is still too scarce to exclude its role, as indeed our experience seems to indicate.

persantine dosing chart 2017-01-18

In this paper, an overview is given of trials with oral anticoagulants and dipyridamole in the secondary prevention after transient ischaemic attack or minor stroke. In patients with atrial fibrillation, the secondary preventive treatment of first choice is oral anticoagulation with an aimed international normalised ratio between 2.0 and 3.0. In patients without a cardiac source of embolism, a combination therapy of low-dose aspirin and dipyridamole 200 mg twice daily is the treatment of choice. These treatment strategies do however not prevent buy persantine all recurrent strokes or vascular complications, and research for more effective strategies is warranted.

persantine 50 mg 2016-04-04

Whether antithrombotic therapy in elderly patients differs from that in younger populations depends on whether the risk for such bleeding differs in the elderly. Regarding long-term therapy with warfarin derivatives, evidence shows that there is a difference. The anticoagulation response to warfarin is exaggerated with advancing age. This article discusses antithrombotic therapies for valvular heart disease, including bioprosthetic and mechanical prosthetic heart valves, aspirin buy persantine and dipyridamole in combination with oral anticoagulant therapy, antiplatelet agents alone or in combination with very low dose warfarin, tilting disk valves, valve position, first-generation valves compared with modern valves, interruption of anticoagulant therapy, and miscellaneous indications for antithrombotic therapy.

persantine generic names 2016-06-02

PPf was significantly correlated to ASI in asymptomatic diabetic patients. Likewise, increased PPf was associated with impaired CFR and subclinical diastolic dysfunction in diabetic patients. PPf buy persantine could be utilized as a simple non-invasive predictor of occult atherosclerosis and diastolic dysfunction in diabetic patients.

persantine drugs 2016-04-07

These recommendations can help clinicians make evidence-based treatment decisions with their patients who have had buy persantine strokes.

persantine drug interactions 2016-11-11

Patients with stress-induced myocardial perfusion defects immediately after successful coronary intervention show high-grade residual stenoses that are more pronounced in patients with perfusion defects than in patients with normal buy persantine postinterventional scintigrams. In addition, vessels serving myocardial regions with perfusion defects showed a significantly higher plaque burden indicating diffuse atherosclerotic changes in the vessel. The evaluation of the postprocedural result by intravascular ultrasound contributes to a better understanding of the discrepancy between the angiographic finding of a widely patent vessel but scintigraphic evidence of impaired perfusion.

persantine dose calculation 2017-02-25

Unlike conventional thallium-201 myocardial imaging, technetium-99m methoxyisobutylisonitrile (MIBI) requires separate stress and rest injections. We prospectively studied 148 consecutive patients referred for myocardial perfusion studies to determine the diagnostic value of rest images once normal exercise or dipyridamole tomographic images had been obtained. In patients referred with no history of previous myocardial infarction in whom the diagnosis of coronary artery disease was suspected, 45 of 109 (41%) patients had normal stress tomographic images. Obtaining rest images did not buy persantine alter the final interpretation in any of these cases. From this we infer that in patients with normal images after exercise or dipyridamole administration and no past history of myocardial infarction, 99mTc-MIBI rest images are not required. This provides several advantages including increased speed of diagnosis, decreased patient radiation exposure, improved cost efficiency and decreased demand on tomographic camera time.

persantine 25 mg 2015-06-09

Nimodipine significantly inhibited the growth of new vessels in rats. The number of nuclei was 310 +/- 69 in the control group (n:14) and 121 +/- 53 in the treated ones (n:14), (p<0.0005). Similar results were found with ginkgo-biloba extracts: 344 +/- 53 (n:15) in controls, and 136 +/- 29 (n:11) in treated ones (p<0.0005), and with dipyridamole: 303 +/- 69 (n:13) in controls, and 131 +/- 48.5 in treated rats (p<0.0005). Results were similar in mice. 186 +/- 45 (n:7) nuclei counted in controls against 90 +/- 25 (n:6) for dipyridamole treated (p<0.0005); and 81 +/- 21 for ginkgo-biloba treated animals (p<0.0005). A gradual, very significant increase in VEGF values in response to relative hypoxia (room air) contrasted with the significant inhibition noted both with ginkgo-biloba extracts and dipyridamole. TGFbeta2 and PDGF both showed a gradual Abilify Maintena Dosing increase in relative hypoxia at days 2 and 4 of room air (p<0.0005). Treated animals showed marked inhibition of the three growth factors.

persantine 10 mg 2017-08-20

The purpose of this study was to determine whether patients at high risk for clinical restenosis, following coronary angioplasty, could be identified by myocardial perfusion imaging performed with dipyridamole- 82Rb Protonix Oral Dosage PET.

persantine 75 mg 2015-11-22

Stroke is associated with elevation of several proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin (IL)-8 that are correlated with central nervous system (CNS) injury. Anti-platelet therapies are important agents in stroke management. The role of antiplatelets as anti-inflammatory agents is not known in acute stroke Imdur 45 Mg patients. Furthermore, their effect on induction of potential cytokines as TNF-alpha and IL-8 in those patients is still not clear. Thus, we herein examined the induction of TNF-alpha and IL-8 in acute stroke patients and examined the effects of the antiplatelets drugs aspirin, clopidogrel and dipyridamole, and piracetam in their induction. Cytokines were detected intracellularly in leukocytes from patients who had first acute ischemic stroke and from matched controls by immunocytochemistry. The results showed significant increase of spontaneously produced TNF-alpha and IL-8 in patients compared to control. This induction was significantly inhibited differently by each drug and dual drug agents. The data of this work suggest that antiplatelets agents may have a role in inhibition of stroke mediated proinflammatory cytokine effects, which may initiate a new aspect of the role of antiplatelets in the treatment of acute ischemic stroke.

persantine drug class 2017-11-27

Increased sympathetic activity contributes to the progression of heart failure. Adenosine counteracts sympathetic activity by inhibition Albenza Medication of presynaptic norepinephrine release and attenuation of the metabolic and contractile responses to beta-adrenergic stimulation. In this study, we tested the hypothesis that the adenosinergic effects (uptake blockade) of dipyridamole may retard the progression of pressure overload hypertrophy in the rat.

persantine generic name 2015-04-16

Patients with peripheral vascular disease have a high prevalence of coronary artery disease and are at increased risk for cardiac morbidity and death after vascular reconstruction. The present study was undertaken to assess the value of 18 clinical Depakote Recommended Dosage parameters, of 7 clinical scoring systems, and of quantitative dipyridamole-thallium imaging for predicting the occurrence of postoperative myocardial infarction or cardiac death. Vascular surgery was performed in 125 patients. Thirteen postoperative cardiac events occurred, including 10 cardiac deaths and 3 nonfatal infarctions. Clinical parameters were not useful in predicting postoperative outcome. All 63 patients with normal scan results or fixed perfusion defects underwent surgery uneventfully, whereas 21% (13/62) of patients with reversible defects had a postoperative cardiac complication. By use of quantitative scintigraphic indexes we found that patients with reversible defects could be stratified into intermediate and high-risk subgroups with postoperative event rates of 5% (2/47) and 85% (11/13), respectively, despite intensive postoperative monitoring and antianginal medication. Thus in patients unable to complete a standard exercise stress test, postoperative outcome cannot be predicted clinically, whereas dipyridamole-thallium imaging successfully identified all patients who had a postoperative cardiac event. By use of quantification we found that patients with reversible defects can be stratified into an intermediate risk subgroup that can undergo surgery with minimal complication rate and a high-risk subgroup that requires coronary angiography.

persantine and alcohol 2015-09-10

Wall motion (WM), Doppler-derived measurement of the coronary flow reserve (CFR) in the left anterior descending coronary artery (LAD), and myocardial perfusion imaging (MPI) can be sequentially assessed during dipyridamole stress echocardiography. Data regarding the relative diagnostic value of each of these parameters when assessed during the same examination in patients with suspected coronary artery disease (CAD) are lacking. Voltaren Arthritis Medication

persantine medication classification 2016-04-28

One thousand Hyzaar Y Alcohol eight hundred consecutive dipyridamole-thallium studies performed between 1985 and 1993 were reviewed to identify 48 subjects who met prespecified selection criteria.

persantine generic 2017-08-01

Coronary vasodilator reserve is often significantly impaired in patients with aortic stenosis by several mechanisms: coronary artery disease, left ventricular hypertrophy, increase in cardiac chamber stiffness. The aim of this study was to Sinemet Online evaluate the feasibility and the diagnostic accuracy of the dipyridamole echocardiography test in the diagnosis of coronary artery disease in patients with aortic stenosis.

cost of persantine 2015-10-07

The accumulation of ZDV in 3T3-F442A cells was rapid, energy dependent, saturable and pH sensitive. Western blot analysis showed that 3T3-F442A cells express P-gp, and direct inhibition assays suggest that ZDV is a substrate of P-gp and MRP.