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At least 973 records · Page 54Linked to original sources
PubMed1986

Potentiation of the antiplatelet action of adenosine in whole blood by dipyridamole or dilazep and the cAMP phosphodiesterase inhibitor, RA 233.

Adenosine (Ado, 10-50 microM), a potent inhibitor of ADP-induced human platelet aggregation in platelet-rich plasma (PRP), does not inhibit aggregation in whole blood. However, the Ado analogs, 2-fluoroadenosine, 2-chloroadenosine and 5'-N-ethylcarboxamidoadenosine (NECA) which are resistant to deamination (2-fluoroadenosine) or deamination and phosphorylation (2-chloroadenosine and NECA), inhibit aggregation in whole blood with IC50 values of 12 microM, 2.3 microM and 0.26 microM, respectively. The inhibitory effect of NECA (200 nM) is potentiated by the platelet cAMP phosphodiesterase (PDE) inhibitor RA 233 (5 microM). Inhibition of the erythrocytic nucleoside transport system by dilazep (1 microM) or dipyridamole (10 microM), or blockade of Ado metabolism by 2'-deoxycoformycin (5 microM) plus 5-iodotubercidin (10 microM), evokes the antiaggregatory action of Ado in whole blood (IC50 congruent to 2 microM). RA 233 (5 microM) potentiates Ado-mediated inhibition about 10-fold when nucleoside transport or Ado metabolism is blocked. Ado (10 microM or 200 nM) is rapidly metabolized within 1 min in whole blood. When nucleoside transport is inhibited by dilazep or dipyridamole, or when Ado metabolism is blocked by 2'-deoxycoformycin and 5-iodotubercidin, 50-60% of the Ado remains in the plasma after 5 min. These results show that the failure of Ado to inhibit platelet aggregation in whole blood results from its rapid uptake and metabolism by erythrocytes. More importantly, these data emphasize the key role of nucleoside transport inhibition in the antiplatelet actions of dipyridamole and dilazep. In addition, superior therapeutic results may be obtained from the combination of blockade of nucleoside transport system with inhibition of platelet cAMP PDE.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1988

Antiplatelet activity of dipyridamole in non anticoagulated whole blood.

Dipyridamole has been reported to inhibit platelet aggregation in citrate anticoagulated whole blood (WB). However, citrate may alter the response of platelets and/or the effect of antiplatelet drugs. The present study evaluates the "ex vivo" effect of dipyridamole, two hours after a single dose (3 mg/Kg) in 25 normal subjects in non-anticoagulated (native) WB and in WB anticoagulated with citrate or hirudin. We have used the BASIC anticoagulated with citrate or hirudin. We have used the BASIC wave as analytical method, which can evaluate the early steps of platelet activation with collagen in less than 1 min after venoclysis, thus allowing the study in native WB. The results show that dipyridamole significantly inhibits (p less than 0.001) platelet activation to collagen in citrated WB (66%) while the drug's effect is much lower (21%) and non-significant if evaluated in native or hirudine anticoagulated WB. These results suggest that citrate or low calcium concentration amplify the drug's platelet inhibitory action in WB and, therefore, the laboratory results may overestimate the drug's effect "in vivo".

Adult↗
PubMed1990

Effect of dipyridamole and aspirin on vein graft patency after coronary bypass operations.

Antiplatelet therapy with dipyridamole, 100 mg q.i.d., starting 2 days before surgery, followed by aspirin, 325 mg t.i.d. plus dipyridamole, 75 mg t.i.d., 7 hours after surgery was assessed in the prevention of saphenous vein bypass graft occlusion. Early (less than or equal to 1 month) and late (1 year) occlusions were reduced both on a per patient and a per distal anastomosis basis. Bleeding complications were not increased. Graft occlusion in high-risk situations (low-flow grafts and endarterectomy) was reduced, but not eliminated, by this antiplatelet regimen. The authors recommend this combination of dipyridamole before surgery, adding aspirin after surgery, to prevent coronary artery bypass graft occlusion.

Aspirin↗
PubMed1990

Dipyridamole in the treatment of angina pectoris: a meta-analysis.

A meta-analysis of 11 randomized trials published between 1960 and 1970 was performed to re-evaluate data on the efficacy of dipyridamole in the prevention and treatment of chronic angina pectoris. Three trials significantly favored drug vs placebo, four showed a trend towards drug vs placebo, two showed no difference and two showed a trend towards placebo vs drug. The combined results of these 11 trials showed a statistically significant improvement with dipyridamole. Although this result should be viewed with caution because of methodologic variations in the studies, the available evidence appears to suggest that dipyridamole may have a beneficial effect, and that it may have been prematurely discarded in the treatment of angina pectoris.

Angina Pectoris↗
PubMed1990

Dipyridamole potentiates the anti-aggregating effect of endothelium-derived relaxing factor.

One effector of the anti-aggregatory property of endothelium is thought to be endothelium-derived relaxing factor. The best characterized of these, nitric oxide, inhibits platelet aggregation by increasing cyclic GMP levels. The effects of nitric oxide and dipyridamole (a cyclic GMP phosphodiesterase inhibitor), alone and in combination, on in vitro platelet aggregation were evaluated. Dipyridamole had no effect per se on platelet aggregation but potentiated the inhibition of aggregation due to nitric oxide. This was concomitant with an increase in platelet cyclic GMP concentration. The author suggests an alternative mechanism for the clinical efficacy of dipyridamole as an antiplatelet agent.

Cyclic AMP↗
PubMed1987

Dipyridamol inhibits activation of human T lymphocytes in vitro.

The effect of dipyridamol on T-lymphocyte activation was investigated. The drug did not have an irreversible toxic effect on T lymphocytes. Dipyridamol inhibited both PHA- and mumps-stimulated proliferation and the proliferative response in mixed lymphocyte cultures. The drug inhibited PHA-stimulated proliferation independent of the time when it was added during the culture period. The PHA-stimulated expression of interleukin-2 (IL-2) receptors and IL-2 production (at least for low concentrations) was not inhibited. Dipyridamol inhibited IL-2-dependent growth of T cell lines. The drug caused no inhibition when present only during antigenic pulsing.

Cell Division↗
PubMed1981

Lack of effect of ischemia and dipyridamole on prostacyclin production in arteriosclerosis obliterans.

Six patients with advanced arteriosclerosis obliterans in the lower extremities were subjected to an exercise test on a tread mill with and without dipyridamole treatment. Prostacyclin (PGI2) release was measured by the concentration of its stable metabolite, 6-keto-prostaglandin F1 alpha in plasma. All the patients suffered from ischemic pain during both tests, but no changes were seen in plasma 6-keto-PGF1 alpha. Dipyridamole did not affect the physical performance. Our results suggest that atherosclerotic vessels do not increase PGI2 production in response to ischemia and that a single dose of dipyridamole does not change PGI2 production.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Ischemic ST-segment changes after dipyridamole infusion.

Thirty consecutive patients were studied by thallium-201 myocardial imaging after dipyridamole infusion and by coronary angiography because of syndromes of chest pain. Eight patients (27%) had ischemic ST-segment changes after the infusion of dipyridamole. They all had significant coronary arterial disease. It is suggested that the combination of visual analysis of myocardial imaging and analysis of ST-segment changes be used after dipyridamole infusion to improve the sensitivity of this non-invasive test.

Adult↗
PubMed1992

Arrhythmias during dipyridamole test. Report of 3 cases.

The authors report three cases in which the dipyridamole test provoked: (1) junctional rhythm with AV dissociation; (2) sinus arrest; (3) 2:1 AV block. The three cases described above draw attention to the possible effect of dipyridamole on the AV conduction, which is not yet completely known. This unwanted effect suggests that careful ECG monitoring should be performed during the dipyridamole test.

Arrhythmias, Cardiac↗
PubMed1994

Coronary spasm induced by dipyridamole during a myocardial scintigraphy.

A 59-year-old male underwent a dipyridamole myocardial scintigraphy. During dipyridamole infusion, a marked ST-segment elevation was observed in the inferior leads. After aminophylline injection, a short burst of ventricular tachycardia occurred, then the ST-segment elevation disappeared. The myocardial scintigraphy was consistent with myocardial ischemia of the inferior wall. The coronary angiography revealed no significant coronary lesion. Coronary spasm induced by dipyridamole remained the most probable mechanism for this complication.

Coronary Vasospasm↗
PubMed1994

Profound shock resulting from a large dose of dipyridamole.

Acute ingestion of more than 200 mg dipyridamole may result in minor symptoms. The reported highest dosage of acute ingestion was 1250 mg. Most experiences of acute ingestion come from dipyridamole thallium image, oral application of 300-400 mg or intravenous 0.56 mg/kg. The systemic or cardiovascular complication could be rapidly reversed by intravenous use of aminophylline, 50-240 mg. We report an experience in dealing with the highest ever dose, 1750 mg, of dipyridamole overdose by usual dose of aminophylline.

Adult↗
PubMed1994

High-grade atrioventricular block during dipyridamole stress testing.

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.

Aged↗
PubMed1995

Doppler determined aortic acceleration after dipyridamole in the prediction of coronary artery disease.

Change in the acceleration of aortic blood flow with stress testing is reported to reflect the presence of myocardial ischaemia. We studied its clinical usefulness when compared with dipyridamole thallium scintigraphy in 101 patients, of whom 64 had coronary angiography. Maximum aortic acceleration increased after dipyridamole (P < 0.0001), although no correlation existed between the aortic acceleration and evidence of thallium perfusion abnormalities. For the patients who had angiography, the increase in aortic acceleration was similar for those with no significant coronary stenoses, single vessel or multi-vessel disease. Compared with coronary angiography, Doppler measurement of maximum aortic acceleration had a sensitivity of 92% and a specificity of 37% for the detection of coronary artery disease. When patients with previous myocardial infarction or left ventricular dysfunction were excluded, there was still no relationship between the maximum aortic acceleration and the presence of coronary artery disease. We conclude that changes in the acceleration of aortic blood flow after dipyridamole stressing do not predict the presence or severity of coronary artery disease as measured from perfusion defects at thallium scintigraphy or by coronary angiography. We have observed a wide variability of aortic maximum acceleration in the evaluation of myocardial ischaemia, which we feel introduces serious limitations to its use in routine clinical practice.

Acceleration↗
PubMed1996

Pharmacological preconditioning of ischemic heart disease by low-dose dipyridamole.

Fourteen patients affected with coronary artery disease underwent two consecutive dipyridamole echocardiographic stress tests, in basal conditions and after repeated low doses of intravenous dipyridamole, following the observation that pulse increases in adenosine plasma levels due to repeated intravenous administration of dipyridamole mimic the mechanism of ischemic preconditioning. Echocardiographic, electrocardiographic, haemodynamic parameters, and adenosine plasma levels were measured. After the second test, six patients were completely negative, and in those eight still positive the onset of dyssynergy was delayed.

Aged↗
PubMed1992

Differential effect of dipyridamole upon thymidine incorporation and expression of surface activation antigens by in vitro stimulated lymphocytes.

Dipyridamole inhibits, by 50% at 10(-6) M and 100% at 10(-5) M, the incorporation of tritiated thymidine by lymphocytes stimulated with 1 microgram/ml phytohaemagglutinin A for 72 h. At the latter concentration, a clinically relevant one, dipyridamole fails to inhibit lymphocyte proliferation and expression of the cell surface stimulation markers, CD25 and HLA-DR, or differential regulation of the CD45 -RA and -RO isoforms, as determined by single laser two-colour flow-cytometry. No significant immunodepressant effect of dipyridamole can be demonstrated in vitro.

Adult↗
PubMed1986

The effect of 3-deazauridine and dipyridamole on uridine utilization by mice.

The inhibition of uridine utilization by 3-deazauridine, an inhibitor of uridine kinase, and by dipyridamole, an inhibitor of the facilitated transport of nucleosides was examined. 3-Deazauridine (500 mg/kg) markedly inhibited (greater than 70%) the formation of uracil nucleotides from uridine in liver, kidney, and L1210 tumor cells. The degree of inhibition is greatly reduced by 6 hr after administration of the drug. Dipyridamole (100 mg/kg) did not significantly reduce salvage of uridine by liver or kidney and produced only small, transient reductions in salvage by L1210 tumors. Dipyridamole pretreatment did not alter the rate of clearance of uridine from the plasma.

3-Deazauridine↗
PubMed1986

Autoradiographic localization of adenosine uptake sites in guinea pig brain using [3H]dipyridamole.

Tritiated dipyridamole, a specific adenosine uptake inhibitor binds in a saturable and reversible fashion to high-affinity receptor sites in guinea pig brain sections (Kd = 10 +/- 1.5 nM; Bmax = 650 +/- 100 fmol/mg prot.). The anatomical distribution of [3H]dipyridamole binding sites obtained with autoradiographic techniques shows a widespread but heterogeneous distribution of the binding sites throughout the whole guinea pig brain. Very high densities of binding sites are observed in the cerebellar cortex (molecular layer), the pyriform cortex, the superior colliculus (superficial layer), the supraoptic nucleus and the nucleus of the tractus solitarius. The anatomical characterization of the adenosine uptake site, using [3H]dipyridamole as a probe, may be useful to determine the functional role of adenosine in the brain.

Adenosine↗
PubMed1992

Dipyridamole induced myocardial recovery after global ischemia.

1. An experimental comparative study on isolated guinea pig hearts was carried out to determine the effect of dipyridamole added to the reperfusion solution on myocardial recovery after global ischemia. 2. After 20 min of normothermic ischemia two groups of solutions: (1) Krebs solution; (2) Krebs + dipyridamole 20 micrograms/l (10 experiments in each group) were used for reperfusion. 3. Postischemic myocardial functions (heart rate, ventricular contractility, heart work) and tissue enzymes (CPK-MB, LDH) were compared with their preischemic values. 4. Addition of dipyridamole 20 micrograms/l to reperfusion solution improved postischemic myocardial functions and decreased myocardial injury.

Animals↗