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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.

persantine medication classification

108 in-patients (mean age 50+/-11 years) with cardiac chest pain underwent dipyridamole stress-Echo with ECG-analysis, wall motion analysis by 2-dimentional imaging (2D) and coronary flow reserve (CFR) evaluation in both LAD and PDA by pulse-wave Doppler. The 2D test was considered positive when more or equal 2 segments demonstrated wall motion abnormalities. CFR was calculated as ratio of hyperemic to basal peak diastolic blood flow velocity. CFR <2.0 was considered reduced. Coronary angiography was performed within one week after stress-Echo.

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Adenosine formation and release were studied in 48-h-old cultured ciliary ganglia and confluent peripheral and CNS glial cultures from embryonic chicks. Metabolic poisoning induced by 30 mM 2-deoxyglucose and 2 micrograms/ml oligomycin reduced ATP concentration by 90%. An increase in adenosine accounted for 15-40% of the fall in ATP. Dilazep (3 X 10(-6) M), a nucleoside transport inhibitor, decreased both incorporation of adenosine (an index of nucleoside transport) and release of adenosine by 80-90%. Dilazep trapped the newly formed adenosine intracellularly. A concentration of alpha, beta-methylene ADP that inhibited ecto-5'-nucleotidase by 80-90% did not alter the concentration of adenosine or AMP in neurons, glia, or medium. The results demonstrate that adenosine is formed intracellularly and exported out of the cell via the nucleoside transporter. The participation of ecto-5'-nucleotidase was excluded.

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Aspirin, sulfinpyrazone and the combination of aspirin/dipyridamole, which inhibit some aspects of platelet function, have been evaluated in large-scale clinical trials in secondary prevention of myocardial infarction. The Persantine-Aspirin Reinfarction Study using dipyridamole, and Anturane Reinfarction Trial and Anturan Reinfarction Italian Study with sulphinpyrazone did not yield conclusive results. There have been five trials in which aspirin has been compared with a placebo. When the results were pooled, the outcome was consistent with a reduction during aspirin treatment of 5-10% in mortality and 20% in coronary event-rate. Whether this small benefit to an individual patient is worthwhile, and whether the effect of aspirin is influenced by coexistent beta-blocker treatment, is not clear.

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This study suggests that an episode of myocardial ischemia is able to change in a dramatic manner the frequency-contained within of the QRS complex, in spite of an unchanged ST segment in the conventional exercise ECG. We suggest that the HFS could be a good method for identifying myocardial ischemia. Its advantages could be important, particularly when the conventional exercise ECG is non informative.

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The most accurate and logistic method of identifying injured but viable myocardium remains a diagnostic challenge.

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To compare the ticlopidine and dipyridamole effects on platelets count and aggregation in patients with stable coronary artery disease.

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Abnormal small coronary artery function may cause limited coronary flow responses to stress, resulting in anginal symptoms and ischemia in some patients with chest pain despite angiographically normal coronary arteries. To assess the exercise hemodynamic correlates of coronary flow abnormalities measured in the cardiac catheterization laboratory, 105 patients with microvascular angina (defined as an increase in coronary vascular resistance during pacing stress after ergonovine administration in the absence of significant epicardial constriction and associated with provocation of the patient's typical chest pain) and 27 patients without any coronary flow abnormality (normal) were analyzed. Of the 105 patients with microvascular angina, 75 had normal electrocardiographic responses to treadmill exercise testing, 22 had ischemic responses, and eight had bundle branch block during exercise. All 27 normal patients had normal electrocardiographic responses to exercise. Patients with ischemic electrocardiographic responses (0 +/- 7%, p less than 0.01), and those with bundle branch block (-2 +/- 6%, p less than 0.01) had abnormal left ventricular ejection fraction responses to exercise compared with the normal group, who demonstrated an 8 +/- 6% increase in left ventricular ejection fraction by radionuclide angiography during exercise, and microvascular angina patients with a normal electrocardiographic response to exercise, who demonstrated a 5 +/- 7% increase in ejection fraction. Although the microvascular response to ergonovine was no different among the three microvascular angina exercise groups, the administration of dipyridamole caused less coronary vasodilation in those patients with apparently ischemic or bundle branch block responses to exercise compared with those with normal electrocardiograms during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

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The involvement of different subtypes of voltage-sensitive (Ca2+ channels in the initiation of field stimulation-induced endogenous adenosine triphosphate (ATP) and [3H]acetylcholine ([3H]ACh) release was investigated in the superfused rat habenula slices. ATP, measured by the luciferin-luciferase assay, and [3H]ACH were released simultaneously from the tissue in response to low frequency electrical stimulation (2 Hz, 2.5 msec, 360 shocks). The N-type Ca(2+)-channel blocker omega-conotoxin GVIA (omega-CgTX, 0.01-1 microM) reduced the stimulation-evoked release of ATP and [3H]ACh in a dose-dependent manner. Similarly, the P-type Ca2+ channel antagonist omega-agatoxin IVA (omega-Aga IVA) (0.05 microM) and the inorganic Ca(2+)-channel blocker Ca2+ (0.2 mM) inhibited the outflow of both transmitters, while Ni2+ (0.1 mM) was without significant effect. A high correlation was observed between the percent inhibition of ATP release and percent inhibition of ACh release caused by the different Ca2+ antagonists. Long-term perfusion (i.e., 90 min) with Ca(2+)-free solution inhibited the evoked-release of ATP and [3H]ACh. In contrast, perfusion of slices with the same media for a shorter time (i.e., 20 min) did not reduce the release of [3H]ACh and ATP but even increased the evoked-release of ATP about fourfold. The breakdown of extracellular ATP was not blocked under low [Ca2+]0 condition, measured by the creatine phosphokinase assay and HPLC-UV technique. Application of extra- or intracellular Ca2+ chelators, and dipyridamole (2 microM), the nucleoside transporter inhibitor, did not reduce the excess release of ATP after short-term perfusion with Ca(2+)-free media. Tetrodotoxin (TTX, 1 microM), while inhibiting the majority of ATP release under normal conditions, was also unable to reduce release under low [Ca2+]0 conditions. In summary, we showed that both N- and P-type Ca2+ channels are involved in the initiation of electrical stimulation-evoked release of ATP and [3H]ACh in the rat habenula under normal extracellular calcium concentration. Under low [CA2+]0 conditions an additional release of ATP occurs, which is not associated with action potential propagation.

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One hundred forty-one subjects with type 2 diabetes mellitus without known cardiac disease and asymptomatic, aged >45 to <76 years, were randomized into the screening arm for CAD (71 patients) or to the control arm (70 patients). The screening consisted in performing an exercise electrocardiogram test and dipyridamole stress echocardiography; if 1 test was abnormal, coronary angiography is done. Screening was positive in 15 subjects (21.4%). At coronary angiography, which was performed in 14 of 15 patients, stenoses > or =50% of vessel diameter were present in 9 patients, of these 4 underwent coronary artery bypass grafting and 4 underwent percutaneous transluminal coronary angioplasty. Stenoses <50% of vessel diameter were present in 5 patients.

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Perfusion imaging showed a reversible perfusion decrease in the hypertrophic septum. Cine-gated imaging of the septum showed dyskinesia and a severe abnormality of systolic thickening during the poststress period, whereas it showed nearly complete recovery at rest. Quantified regional perfusion and function indices also showed this perfusion decrease and myocardial dysfunction after dipyridamole stress.

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To assess the feasibility, safety and usefulness of gradient-echo magnetic resonance imaging (MRI) combined with pharmacologic stress testing for the detection of coronary artery disease, 23 patients without previous myocardial infarction but with significant stenosis (greater than 70% diameter stenosis) of greater than or equal to 1 major coronary artery were selected for dipyridamole-MRI stress testing. Each patient underwent MRI at rest, and high-dose dipyridamole-MRI (0.75 mg/kg over 10 minutes) of corresponding basal and midventricular short-axis tomograms. Additionally, these patients performed symptom-limited exercise stress tests. All short-axis tomograms were evaluated on a standardized segmental basis by grading each segment as normal, hypokinetic, akinetic or dyskinetic. Dipyridamole-MRI was considered pathologic if segmental wall motion deteriorated by greater than or equal to 1 grade after dipyridamole. For comparison with coronary angiography, segmental wall motion gradings were related to the respective coronary artery territories in the short-axis plane. Pathologic dipyridamole-MRI was obtained in 18 of 23 (78%) patients. For 1- and 2-vessel diseases, sensitivity was 69 and 90%, respectively. Exercise stress tests were pathologic in 14 of 23 (66%) patients. For 1- and 2-vessel diseases, sensitivity of exercise stress test was 58% (7 of 12 patients) and 77% (7 of 9), respectively. Sensitivity/specificity of dipyridamole-MRI for the localization of the stenosed coronary artery was 78/100% for left anterior descending, 73/100% for left circumflex, and 88/87% for right coronary artery stenoses. It is concluded that dipyridamole-MRI is a feasible nonexercise-dependent test for detection and localization of functionally significant coronary artery disease.

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Nitrate tolerance remains a problem despite an enormous number of studies on this phenomenon. The aim of the present study was to compare the efficacy of nitroglycerin transdermal patches intermittently or continuously administered to patients with myocardial ischemia evaluated by the echocardiography dipyridamole stress test. We prospectively studied 34 coronary patients with stable myocardial ischemia. A double-blind, randomized, crossover study technique was used. After a run-in period (1 week) they underwent a dipyridamole stress test to evaluate nitrate responsiveness and then were randomized to 1 week of transdermal nitroglycerine 20 mg/24 h (two patches of 10 mg/24) administered either intermittently or continuously for 1 week. During the following week all patients were given placebo. In the final week, therapy was crossed over the alternate regimen. No significant changes in heart rate, systolic and diastolic blood pressure and rate-pressure product were observed at basal conditions and at peak of dipyridamole infusion among patients after placebo run-in period, after acute, 1 week of intermittent and 1 week of continuous nitroglycerine administration. At peak of dipyridamole infusion after acute administration of nitrate we observed a significant decrease in wall motion score index with respect to placebo. This pattern was similar during intermittent, but not continuous, patch therapy (p < 0.001). Our results suggest that transdermal nitroglycerin patches are an effective anti-ischemic medication, in reducing transient myocardial ischemia induced by dipyridamole. This anti-ischemic effect is lost when an overnight nitrate free dose interval is not used. Moreover the dipyridamole echocardiographic stress test, besides evaluating myocardial ischemia-induced wall motion abnormalities, is adequate to assess both the efficacy and the tolerance of transdermal nitrate therapy.

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In this study, 1001 patients with documented coronary artery disease by coronary arteriography showing any visible coronary artery narrowing underwent rest-dipyridamole PET perfusion imaging. Quantitative severity of dipyridamole-induced, circumscribed, segmental PET perfusion defects was objectively measured by automated software as the minimum quadrant average relative activity indicating localized flow limiting stenoses. Quantitative severity of the graded, longitudinal, base-to-apex myocardial perfusion gradient indicating fluid dynamic effects of diffuse coronary artery narrowing was objectively measured by automated software as the spatial slope of relative activity along the cardiac longitudinal axis.

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These results suggest that dipyridamole, a potent coronary vasodilator, produces maldistribution of coronary blood flow in our dog models, whereas sevoflurane does not do this in animal or human studies.

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To investigate the value of the echocardiographic observation of the left ventricular hypertrophy (LVH) in diagnosing myocardial microvascular damage in patients with essential hypertension (EH).

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The precore mutation rate was 10/12. The therapeutic effect of the immune therapy on the precore mutation patients (5/7) was better than that on the HBsAg(+), HBeAg(+) patients (2/11), P less than 0.05.

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Caffeine binds to the A2 receptors and inhibits adenosine's action of vasodilation or dipyridamole-induced vasodilation. Patients scheduled for (201)Tl myocardial perfusion using pharmacologic stress with dipyridamole or adenosine are advised to abstain from caffeine for 24 h before the test. This article reports on the residual serum caffeine levels of 36 patients after 24-h caffeine abstention and the clinical implications on dipyridamole (201)Tl myocardial perfusion imaging.

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Aqueous and vitreous samples were obtained from bovine eyes after death and from live porcine eyes with the subject under general anesthesia. Samples from live eyes were immediately incubated in the sampling syringe with pentoxifylline, erythro-9-(2-hydroxy-3-nonyl) adenine, and dipyridamole to prevent synthesis or degradation of adenosine during the collection procedure, filtered, and flash-frozen in liquid nitrogen. All samples were then filtered and purified on phenylboronate agarose columns and incubated with chloroacetaldehyde to convert the adenosine present in the sample to the fluorescent derivative 1,N6-ethenoadenosine. The 1,N6-ethenoadenosine was separated by high-pressure liquid chromatography and then measured by fluorometry.

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We investigated the postoperative prognostic value of preoperative myocardial SPECT for predicting clinical outcomes, including event-free survival and functional improvement.

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During continuous exposure, cells were more responsive to doxorubicin (DOX) in the presence of dipyridamole (DPM). Translocation of nucleolar phosphoprotein B23 and inhibition of cell growth occurred with a lower dose of DOX and in a shorter incubation time in the presence of DPM. DPM did not change translocation induced by actinomycin D (Act-D). Short exposure of HeLa cells to Act-D induced "reversible" translocation of protein B23 as well as "reversible" inhibition of cell growth. DPM included in the cell culture after removal of Act-D inhibited the recovery of cell growth as well as the corresponding relocalization of protein B23 from the nucleoplasm to nucleoli. DPM administered in the fresh medium after 30 min exposure to DOX had little effect on the potentiation of the induced translocation of protein B23 and inhibition of cell growth. Our results indicated that "B23 translocation" is closely associated with states of cell growth. The potentiation of the inhibition of cell growth by DPM is associated with the extent of enhanced protein B23 translocation. "B23 translocation" may therefore be a simple and rapid method for assessing the inhibition of cell growth and for determining the efficacy of combination cancer chemotherapy.

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Dipyridamole stress testing may be used in the diagnosis of coronary artery disease and risk assessment of patients who are unable to exercise. Although dipyridamole perfusion imaging has a good safety record, serious side-effects may rarely occur. We present a case in which dipyridamole induced high-grade atrioventricular (AV) block that responded promptly to intravenous aminophylline but not to atropine.

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The presence of allele 'a' may be a risk factor for microvascular endothelial dysfunction and higher TFCs in SCF patients.

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Thirty patients with valvular disease confirmed by echocardiography underwent 99mTc-MIBI myocardial perfusion imaging using multiSPECT 1h after stress test (exercise, dipyridamole or dobutamine test) and were performed coronary angiography within 1 month before valvular operation.

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Acetylcholine (ACh) is a major excitatory neurotransmitter in the myenteric plexus, and it regulates its own release acting via muscarinic autoreceptors. Adenosine released from stimulated myenteric neurons modulates ACh release preferentially via facilitatory A(2A) receptors. In this study, we investigated how muscarinic and adenosine receptors interplay to regulate ACh from the longitudinal muscle-myenteric plexus of the rat ileum. Blockade of the muscarinic M(2) receptor with 11-[[2-1[(diethylamino) methyl-1-piperidinyl]- acetyl]]-5,11-dihydro-6H-pyrido [2,3-b][1,4] benzodiazepine-6-one (AF-DX 116), 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and atropine facilitated [3H]ACh release evoked by short stimulation trains (5 Hz, 200 pulses). Prolonging stimulus train length (>750 pulses) shifted muscarinic autoinhibition towards facilitatory M(3) receptors activation, as predicted by blockade with J104129 (a selective M(3) antagonist), 4-DAMP and atropine, whereas the selective M(2) antagonist, AF-DX 116, was without of effect. Blockade of A(2A) receptors with ZM 241385, inhibition of adenosine transport with dipyridamole, and inhibition of ecto-5'-nucleotidase with concanavalin A, all attenuated release inhibition caused by 4-DAMP. J104129 and 4-DAMP, but not AF-DX 116, decreased ( approximately 60%) evoked adenosine outflow (5 Hz, 3000 pulses). Oxotremorine (300 micromol L(-1)) facilitated the release of [3H]ACh (34 +/- 4%, n = 5) and adenosine (57 +/- 3%, n = 6) from stimulated myenteric neurons. 4-DAMP, dipyridamole and concanavalin A prevented oxotremorine-induced facilitation. ZM 241385 blocked oxotremorine facilitation of [3H]ACh release, but kept adenosine outflow unchanged. Thus, ACh modulates its own release from myenteric neurons by activating inhibitory M(2) and facilitatory M(3) autoreceptors. While the M(2) inhibition is prevalent during brief stimulation periods, muscarinic M(3) facilitation is highlighted during sustained nerve activity as it depends on extracellular adenosine accumulation leading to activation of facilitatory A(2A) receptors.

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Forty-eight patients were randomized to adenosine or dipyridamole cardiac stress (82)RB-PET. Respiratory rates and depths were measured by a respiratory gating system in addition to registering actual respiratory rates. Patients undergoing adenosine stress showed a decrease in measured respiratory rate from initial to later scan phase measurements [12.4 (±5.7) vs 5.6 (±4.7) min(-1), P < .001] and tended to have a lower frequency of successful respiratory gating compared to dipyridamole (47% vs 71%, P = .12). As a result, imaging quality was superior in the dipyridamole group compared to adenosine.

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persantine drug class 2015-08-28

To report a case of fulminant shock and noncardiogenic pulmonary edema induced by buy persantine intravenously administered dipyridamole.

persantine generic names 2016-04-17

N6-Methyladenosine strongly stimulates [1-14C]glucose oxidation in rat adipocytes [J.E. Souness and V. Chagoya de Sanchez, Fedn Eur. Biochem. Soc. Lett. 125, 249 (1981)]. The effect of the adenosine analogue is largely independent of its action as an R-site agonist. Removal of endogenous adenosine was a prerequisite for the manifestation of the effect of N6-methyladenosine. Nucleoside uptake inhibitors, dipyridamole and nitrobenzylthioinosine, did not block the action of N6-methyladenosine on [1-14C]glucose oxidation. The effect of the adenosine analogue was not greatly influenced by N6-phenylisopropyladenosine, nicotinic acid or theophylline. Although buy persantine N6-methyladenosine stimulated 3-O-methylglucose uptake into fat cells, it is uncertain whether this was its only effect on glucose metabolism, in view of the comparable enhancement of hexose transport elicited by N6-phenylisopropyladenosine, a much weaker stimulator of glucose oxidation. That hexose transport is not the sole site of action of N6-methyladenosine was supported by the finding that, under conditions which have been proposed to make glucose transport rate limiting, the adenosine analogue only weakly enhanced [1-14C]glucose oxidation. The conversion of glucose carbon 1 to 14CO2 was enhanced by N6-methyladenosine to a greater degree than that of carbon 6, suggesting an increase in pentose phosphate shunt activity. Mechanisms by which this could arise are discussed. Although similarities exist between the effects of insulin and N6-methyladenosine on adipocyte glucose metabolism, the mechanisms by which they stimulate glucose oxidation appear to be distinct, in view of the additivity of their actions on [1-14C]glucose conversion to 14CO2. The results indicate that N6-methyladenosine affects fat-cell glucose metabolism via two different mechanisms: (1) a weak R-site-dependent mode of action related to stimulation of glucose transport and inhibition of lipolysis, and (2) a strong R-site-independent effect of unknown mechanism.

persantine dosing chart 2015-06-22

When wall motion abnormality is the diagnostic end point, concomitant antiischemic therapy heavily modulates the prognostic value of dipyridamole echocardiography test (DET). A negative test result is less benign, and a positive test result is more malignant if performed under therapy. Recently, coronary flow reserve (CFR) was added to wall motion in dual imaging DET. The aim of the study was to determine whether antianginal medications affect the prognostic value of Doppler echocardiographic-derived CFR in patients with known buy persantine or suspected coronary artery disease undergoing DET.

persantine tablets 2016-02-25

The authors sought to determine the best value of Doppler-echocardiography-derived coronary flow reserve (CFR) for detecting ≥75% stenosis of the left anterior descending artery (LAD) and assessing the risk in patients with and without hypertension. Participants The study group was formed by 2089 patients (1411 hypertensive patients and 678 normotensive patients) with known buy persantine or suspected coronary artery disease who underwent dipyridamole (up to 0.84 mg/kg over 6 min) stress echo with CFR assessment of LAD by Doppler and coronary angiography.

persantine 75 mg 2016-01-17

Dipyridamole is a widely prescribed drug in ischemic disorders, and it is here investigated for potential clinical use as a new treatment for breast cancer. Xenograft mice bearing triple-negative breast cancer 4T1-Luc or MDA-MB-231T cells were generated. In these in vivo models, dipyridamole effects were investigated for primary tumor growth, metastasis formation, cell cycle, apoptosis, signaling pathways, immune cell infiltration, and serum inflammatory cytokines levels. Dipyridamole significantly reduced primary tumor growth and metastasis formation by intraperitoneal administration. Treatment with 15 mg/kg/day dipyridamole reduced mean primary tumor size by 67.5 % (p = 0.0433), while treatment with 30 mg/kg/day dipyridamole resulted in an almost a total reduction in primary tumors (p = 0.0182). Experimental metastasis assays show dipyridamole reduces metastasis formation by 47.5 % in the MDA-MB-231T xenograft model (p = 0.0122), and by 50.26 % in the 4T1- buy persantine Luc xenograft model (p = 0.0292). In vivo dipyridamole decreased activated β-catenin by 38.64 % (p < 0.0001), phospho-ERK1/2 by 25.05 % (p = 0.0129), phospho-p65 by 67.82 % (p < 0.0001) and doubled the expression of IkBα (p = 0.0019), thus revealing significant effects on Wnt, ERK1/2-MAPK and NF-kB pathways in both animal models. Moreover dipyridamole significantly decreased the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in primary tumors (p < 0.005), and the inflammatory cytokines levels in the sera of the treated mice. We suggest that when used at appropriate doses and with the correct mode of administration, dipyridamole is a promising agent for breast-cancer treatment, thus also implying its potential use in other cancers that show those highly activated pathways.

persantine generic name 2015-05-22

Intravenous administration of aminophylline is widely adopted to reverse dipyridamole-related adverse effects (AEs) during stress myocardial perfusion imaging (MPI). The study aimed to buy persantine investigate the efficacy of lower-dose aminophylline to relieve minor AEs.

persantine dosage chart 2017-03-31

A prospectively compiled computerized database of all primary eCEAs performed at a tertiary referral center between September 1998 and December 2009 was analyzed. The end point buy persantine was any neck bleeding after eCEA. End point predictors were identified by univariate analysis.

persantine cost 2016-12-15

Antithrombotic and thrombolytic agents form the cornerstone of stroke prevention and treatment. Large, randomized trials have also highlighted the effectiveness and safety of early and continuous antiplatelet therapy in reducing atherothrombotic stroke recurrence. Aspirin is the antiplatelet treatment standard against which several other antiplatelet agents (ticlopidine, clopidogrel, aspirin-dipyridamole) have been shown to be more effective. The prevention of cardioembolic stroke is best accomplished with oral anticoagulation, barring any contraindications. The thrombolytic agent, rt-PA, improves outcome in ischemic stroke patients treated buy persantine within 3 hours of onset. The risk-benefit ratio is narrow because of an increased risk for bleeding but studies do not support a higher risk in the geriatric population.

persantine medication 2017-08-21

Intravenous dipyridamole was given for routine thallium-201 myocardial perfusion imaging. The patient developed chest discomfort followed by cardiovascular buy persantine collapse with sinus arrest and a nodal escape rhythm at 28 beats per minute. He was rapidly resuscitated without adverse sequelae. A reversible posteroinferior perfusion defect and proximal right coronary artery occlusion were found. Symptomatic bradycardia after dipyridamole may be mediated by ischaemia.

persantine dose calculation 2015-10-12

1. The effects of adenosine deaminase, inosine, alkylxanthines (8-phenyltheophylline (8-PT), theophylline and isobutylmethylxanthine (IBMX], dipyridamole, alpha, beta-methylene ADP (AOPCP) and ATP analogues (alpha, beta-methylene ATP and beta, gamma-methylene ATP) on evoked end-plate potentials (e.p.p.s) were investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with tubocurarine. The effects of 8-PT and IBMX on the amplitude and quantal content of e.p.p.s were also investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with high-magnesium solutions. 2. Adenosine deaminase reversibly increased the amplitude of e.p.p.s and prevented the reduction caused by exogenously applied adenosine on e.p.p. amplitude. The increase caused by adenosine deaminase was equivalent to the decrease caused by 12 +/- 5.8 microM-adenosine on e.p.p. amplitude. 3. Inosine, the product of adenosine deamination, was virtually devoid of effect on e.p.p.s. 4. The adenosine receptor antagonists at the frog neuromuscular junction, 8-PT and theophylline, increased in a concentration-dependent manner the amplitude of e.p.p.s in the presence of tubocurarine. 8-PT buy persantine increased the amplitude and quantal content of e.p.p.s in the presence of high magnesium. IBMX, which does not behave as an adenosine receptor antagonist at the frog neuromuscular junction, decreased the amplitude of e.p.p.s in the presence of tubocurarine or high-magnesium solutions. 5. Dipyridamole, an adenosine uptake blocker, decreased the amplitude of e.p.p.s, and in a concentration that did not affect neuromuscular transmission potentiated the depressing effect of adenosine, but not that of 2-chloroadenosine, on the amplitude of e.p.p.s. 6. AOPCP, an inhibitor of 5'-nucleotidase, increased the amplitude of e.p.p.s and markedly attenuated the depressing effect of ATP, but not that of adenosine, on e.p.p. amplitude. 7. The ATP analogue, alpha, beta-methylene ATP, which is not a substrate for 5'-nucleotidase, was virtually devoid of effect on e.p.p.s. beta, gamma-Methylene ATP, which can be a substrate for 5'-nucleotidase, mimicked the depressing effect of ATP on e.p.p. amplitude, an effect which was also reduced by AOPCP. 8. It is concluded that in conditions in which the initial quantal content is assumed to be normal (1) endogenous adenosine depresses neuromuscular transmission, (2) at the neuromuscular junction adenosine is inactivated through a dipyridamole-sensitive uptake process, and (3) released adenine nucleotides might contribute to the pool of endogenous adenosine which modulates neuromuscular transmission.

persantine and alcohol 2015-03-06

The purpose of this review was to discuss results from clinical trials that have compared the efficacy of ASA monotherapy versus ASA + extendedrelease dipyridamole in secondary buy persantine stroke prevention.

persantine overdose 2015-10-24

After uncomplicated myocardial infarction, clinical and ergometric data before hospital discharge allow identification of patients at high risk of further cardiac events. These relate to the necrosed myocardium (left ventricular dysfunction, sometimes latent, and arrhythmia risk), and also to the buy persantine jeopardized myocardium: the moderate sensitivity and specificity of classical exercise stress testing for the detection of this often silent ischaemia are much improved by stress radionuclide and echocardiographic techniques (exercise, dipyridamole, dobutamine. . .), the large scale indications of which remain to be validated.

persantine medication classification 2017-07-21

HPMCs were cultured from human omentum by an enzyme buy persantine digestion

persantine drug 2015-02-15

Serum antithrombin activity (AA) was correlated with coronary angiographic findings in 69 patients with documented angina. There was excellent correlation between normal values and normal coronary circulation or only one-vessel stenosis in 30 of 35 patients (86%). When AA was above 90%, 90% of patients (20 of 22) had normal circulation or one-vessel occlusion. In 24 patients AA values were significantly decreased. Coronary angiography in this group revealed three with normal circulation or only one-vessel involvement (10%); 21 of 24 had two or three vessels Deltasone With Alcohol occluded (90%). The correlation between severe CAD and low AA is probably coincidental to a "triggered" or "turned-on" clotting system. The most practical clinical contribution of AA estimation relates to this capacity to identify angina patients in whom clot-preventive measures (aspirin; dipyridamole; anticoagulants) might prove beneficial.

persantine dosage 2016-07-16

Patients with Biaxin Liquid Dosage abnormal HR response were more frequently without chest pain, with a history of chronic renal failure and taking digoxin. Baseline HR was higher and had fewer symptoms during stress. The stress and rest perfusion defects were greater, but reversibility was not; in addition, LVEF was lower. Multivariable logistic regression analysis demonstrated that the independent predictors of abnormal HR response were baseline HR and low LVEF.

persantine oral dose 2016-03-15

An experimental model of angina pectoris has been developed in order to study the hemodynamic, metabolic and electrophysiological alterations of the heart assumed to occur in the human disease and to analyze the influence of nitroglycerin and dipyridamole on the above changes. In anesthetized and thoractomized dogs, the left anterior descending coronary artery was autoperfused from the subclavian artery. Coronary blood flow was reduced until the epicardial monopolar electrocardiogram recorded from the myocardial segment supplied by the constricted coronary artery was just short of ischemic changes. O2 consumption and lactate uptake of the same segment were determined from the arteriovenous difference by sampling venous blood draining this area. Increasing heart rate by Tofranil 10 Mg 50 to 70 beats/min by electrical pacing of the right atrium evoked a reversible and reporducible elevation of the ST segment and T wave of the electrocardiogram. Blood flow to the area perfused by the constricted coronary artery as well as the O2 uptake of the same area failed to increase on pacing. A concomitant decrease of lactate uptake, sometimes becoming even negative, was indicative of ischemia of that area. These changes could be reduced or prevented by a 10-minute infusion of a total dose of 20 mug/kg of nitroglycerin but not by 60 mug/kg of dipyridamole. Since the changes are fully reversible and readily reproducible, and the response also appears to show parallelisms with those observed in the human patient during an acute angina pectoris attack, use of this model for the assay of antianginal drugs seems to be warranted.

persantine 25 mg 2015-06-18

Acetone is proposed as an isolating agent for extraction of dipyridamolum from biological Moduretic Fluid Tablets material. Optimal conditions of isolating dipyridamolum from human cadaveric liver tissue with acetone are determined and quantitative estimation of isolation results is provided.

persantine 25mg tabs 2017-05-18

Coronary flow velocities were measured in 15 pigs using a Doppler flow wire. The effect of increasing glibenclamide concentrations (0.1-10 microM) on adenosine-induced coronary flow reserve was examined in five animals. Ten pigs served Augmentin Cystitis Dosage as time controls. The time controls were subsequently treated by 3 microM glibenclamide (n = 5) or corresponding vehicle (n = 5) and the flow response to 0.56 mg/kg dipyridamole determined.

persantine brand name 2016-01-19

Platelet-inhibiting drugs have been used widely in the treatment of thrombotic thrombocytopenia purpura. Nineteen consecutive patients received various treatments including platelet inhibitors, glucocorticoid drugs, whole blood or plasma exchange transfusions, and splenectomy. During treatment with aspirin and dipyridamole in 14 patients, five died, and only one Rulide Medication Ingredients had neither new neurologic signs nor worsening thrombocytopenia. Prostacyclin in one patient was not beneficial. Serious bleeding complications, including massive upper gastrointestinal hemorrhage, epistaxes, or subarachnoid hemorrhage confirmed at autopsy, occurred in five of the 19 patients and only during treatment with aspirin and dipyridamole. We conclude that there is no evidence for the effectiveness of aspirin and dipyridamole in the treatment of thrombotic thrombocytopenic purpura and that these drugs may increase the risk of serious bleeding complications.

persantine drug interactions 2017-12-05

In comparison with placebo, dipyridamole less frequently induced chest pain (20% vs. 100%, p = 0.001) and >0.1 mV ST segment depression (50% vs. 100%, p < 0.05). Wall motion abnormalities during exercise-stress test were less frequent (placebo = 100% vs. dipyridamole = 70%, p = ns) and significantly less severe (wall motion score index at peak stress: placebo = 1.55 +/- 0.17 vs. dipyridamole = 1.27 +/- 0.2, p < Zyrtec Overdose 0.01) following dipyridamole, which also determined an increase in exercise time up to echocardiographic positivity (placebo = 385.9 +/- 51.4 vs. dipyridamole = 594.4 +/- 156.9 s, p < 0.01).

persantine drug classification 2016-09-06

The cardioprotective effects Motilium Dose Infantil of nifedipine, verapamil, diltiazem, bepridil, CERM 11956, lidoflazine, mioflazine and the coronary vasodilator dipyridamole were evaluated in the guinea-pig working heart with respect to cardiac function and high energy phosphate content after 45 min of global ischaemia and 25 min of reperfusion. All drugs, with the exception of dipyridamole, induced a negative inotropic effect, which resulted in a decrease of the aortic pressure (AoP), of its first derivative dAoP/dt and the cardiac output. To compare the anti-ischaemic effect of the calcium antagonists, concentrations were selected that reduced the dAoP/dt by 10% (EC10) and 30% (EC30), respectively. With the exception of nifedipine at the EC10 and bepridil and CERM 11956 at the EC30, perfusion with the calcium antagonists and dipyridamole (3 mumol/l) improved the recovery of contractile function after global ischaemia and reperfusion to a value between 60 and 80% of the controls in normoxic hearts. Pretreatment with nifedipine, verapamil, diltiazem, lidoflazine and mioflazine, but not with bepridil, CERM 11956 and dipyridamole led to slightly increased ATP levels in ischaemic hearts as compared to the control value in ischaemic hearts. After subsequent reperfusion for 25 min, for all drugs, ATP levels were further enhanced to 50% of the level in normoxic hearts; phosphocreatine levels reached normoxic values. In particular at the EC30, the effects of calcium antagonists on cardiac function varied in accordance with their known pharmacological and physiological profile. However, there appeared to exist no direct relationship between their beneficial effects on contractile activity and those on the levels of high energy phosphates after ischaemia and reperfusion.

persantine generic 2017-03-31

Reduced HR response was found in 78 % of patients. Patients with abnormal HR response were more frequently had a history of diabetes mellitus, chronic renal failure, and had lower high-density lipoprotein (HDL) levels. Peak HR, SSS, SRS, sLVEF and rLVEF were lower; rest HR, RTS, and the number of patients with ≤ 45 % sLVEF and Zocor Cold Medicine rLVEF were higher in reduced HR response group (all p < 0.05). There was no difference between groups by means of gender, rest and peak systolic or diastolic tension, SDS, SMS, STS, RMS, history of hypertension, peripheral arterial disease, metabolic syndrome, coronary interventions, digoxin, calcium channel blocker or beta blocker usage. Multivariable logistic regression analysis demonstrated that the independent predictors of reduced HR response were HDL, rest HR and SSS. When HDL was removed from the model, chronic renal failure also emerged as an independent predictor.

persantine drugs 2015-12-15

2204 consecutive patients who underwent DSE (n=1093), Bactrim Dosage Peds DiSE (n=394), or DTS (n=717) testing before major vascular surgery were studied.