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PubMed1981

Effects of very low versus standard dose acetyl salicylic acid, dipyridamole and sulfinpyrazone on platelet function and thromboxane formation in man.

The effects of three conventional antiplatelet regimes, dipyridamole 3 X 75 mg/day (D), sulfinpyrazone 4 X 200 mg/day (S), acetylsalicylic acid 3 X 330 mg/day combined with dipyridamole 3 X 75 mg/day (ASA + D), and very low dose acetylsalicylic acid 100 mg/day (ASA) on platelet function were studied in man following 4 days of treatment. D and S slightly increased mean minimal ADP concentration for irreversible aggregation (n.s.), S reduced aggregation and thromboxane (TXB2) formation on low dose collagen (2P less than or equal to 0.05), ASA and ASA + D increased platelet count (2P less than or equal to 0.05), increased bleeding time (n.s. for ASA, 2P less than or equal to 0.05 for ASA + D), abolished irreversible aggregation on ADP, suppressed TXB2 formation on all (2P less than or equal to 0.001) and aggregation on lower concentrations of collagen (2P less than or equal to 0.01) and abolished aggregation and TXB2 formation on arachidonic acid (2P less than or equal to 0.001). Very low dose ASA suppresses platelet aggregation and TXB2 formation on several stimuli of possible physiologic significance. In the light of a recently proposed critical balance of vascular antiaggregatory prostacyclin and platelet proaggregatory TXA2 very low dose ASA might offer advantages over conventional dosage of ASA and should be evaluated in thromboembolic disorders.

Adenosine Diphosphate↗

PubMed1984

Purine receptors in trachea: studies with adenosine deaminase and dipyridamole.

ATP, adenosine, adenine and inosine exhibited similar potency in relaxing transverse strips of guinea-pig trachea. Dipyridamole potentiated responses to ATP and adenosine equally but antagonized responses to inosine and failed to affect responses to adenine. In dipyridamole-treated preparations, adenosine deaminase markedly reduced responses to ATP and adenosine; responses to adenine and inosine were unaffected. The results suggest that ATP acts via its adenosine metabolite and that inhibitory ATP receptors are absent.

Adenosine↗

PubMed1984

Model system to study interaction of platelets with damaged arterial wall. I. Inhibition of platelet adhesion to subendothelium by aspirin and dipyridamole.

An experimental model system has been developed to study the interaction of platelets with a damaged vessel wall, in vivo, without deep surgical intervention. Endothelium of the central ear artery of an anesthetized rabbit is damaged by placing artery forceps on the ear directly over the vessel. Forceps are removed 30 min later and blood flow resumes. After 30 min, blood is washed out with Tyrode's solution and the vessel is perfused with 1% glutaraldehyde solution. Tissue containing the vessel is then removed and further prepared for scanning and transmission electron microscopy. Damage to the endothelium observed by scanning electron microscopy included separation of adjacent endothelial cells (EC); partial destruction and lifting up of some EC, exposing subendothelium; and denudation of larger areas of endothelium. Disc-shaped platelets were seen clinging to some damaged endothelial cells. Platelets adhered, formed pseudopods, and spread over the surface of some areas of exposed subendothelium. The extent of platelet adhesion to exposed subendothelium was estimated by eight "blind" evaluators and the average taken. Aspirin (8 mg/kg, ip) significantly inhibited adhesion (P less than 0.05) when compared to controls. No other agent tested gave significant inhibition after a single treatment. Dipyridamole (1.5 mg/kg, ip) given five times on 3 successive days, inhibited adhesion significantly (P less than 0.001). Heparin (800 U/kg, iv) or dipyridamole (0.7 mg/kg, ip) enhanced the inhibitory effect of aspirin (8 mg/kg, ip), with either combined treatment giving P less than 0.001.

Animals↗

PubMed1986

The role of aspirin and dipyridamole on vascular DNA synthesis and intimal hyperplasia following deendothelialization.

Platelets are implicated both in acute thrombotic events and, through platelet-derived growth factor, in the development of intimal hyperplasia. We have investigated, in vivo, the influence of aspirin and dipyridamole on vascular smooth muscle cell proliferation and DNA synthesis following balloon catheter injury. Fifty-eight male, New Zealand white rabbits were divided equally into two groups; the test group was fed aspirin (14 mg/kg/day) and dipyridamole (9 mg/kg/day) from 2 days prior to surgery until sacrifice at 1, 2, 3, 4, 7, 14, or 28 days after injury. All animals were sacrificed 1 h after injection of [3H]thymidine and the smooth muscle cell DNA specific activity and total kinetic activity were determined. Intimal hyperplasia was measured by light microscopy and intimal nuclear proliferation was determined by counting nuclei per millimeter of internal elastic lamina. Nuclear proliferation was maximal at 14 days (25 +/- 1.2) but intimal hyperplasia was still increasing at 28 days. DNA specific activity after 24 hr (test: 4 +/- 2 dpm/micrograms DNA; control: 3.3 +/- 3 dpm/micrograms DNA) was similar to basal levels in uninjured rabbits. DNA synthesis peaked in both groups between the second and third day (test: 177 +/- 27 dpm/micrograms DNA; control: 185 +/- 39 dpm/micrograms DNA) and then declined slowly toward baseline values. There was no significant difference between treated and normal rabbits in either [3H]thymidine incorporation, nuclear proliferation, or development of intimal hyperplasia despite 90% inhibition of platelet aggregation and a significant reduction (78%) in [14C]serotonin release following collagen challenge (6 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Postirradiation administration of adenosine monophosphate combined with dipyridamole reduces early cellular damage in mice.

The administration of dipyridamole and adenosine 5'-monophosphate (AMP) to mice 5 to 25 min after 1 Gy of total-body gamma irradiation was found to decrease cellular damage, as indicated by the thymidine level in plasma and the amount of saline soluble polynucleotides in the thymus. The drug combination used did not influence similar cytotoxic effects of hydrocortisone. Furthermore, it was shown that the addition of dipyridamole and AMP to in vitro irradiated suspensions of thymocytes enhanced the rejoining processes of DNA strand breaks. Receptor-mediated action of extracellular adenosine may be responsible for the therapeutic effects observed.

Adenosine Monophosphate↗

PubMed1993

Effects of dipyridamole and R-verapamil on in vitro proliferation of blast cells from patients with acute myelogenous leukaemia.

Cytokine-dependent AML cell proliferation was investigated in 16 patients. Dipyridamole and R-verapamil caused a dose-dependent inhibition of AML cell proliferation, and for both drugs the degree of inhibition was similar when testing various haematopoietic growth factors or growth factor combinations (IL3, G-CSF, GM-CSF, G-CSF + GM-CSF, TNF-alpha + GM-CSF). TNF-alpha alone increased AML cell proliferation for five patients, whereas four patients showed unaltered or decreased proliferation. Independent of this TNF-alpha effect, R-verapamil inhibited proliferation for all AML patients in the presence of TNF-alpha, whereas dipyridamole caused only a weak inhibition.

Adult↗

PubMed1990

Symptomatic bradycardia complicating the use of intravenous dipyridamole for thallium-201 myocardial perfusion imaging.

Intravenous dipyridamole was given for routine thallium-201 myocardial perfusion imaging. The patient developed chest discomfort followed by cardiovascular 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.

Bradycardia↗

PubMed1992

Radiosensitizing and repair-inhibiting properties of dipyridamole.

Radioresistance and postirradiation repair of potentially lethal damage (PLD repair) are important factors underlying failure to control local disease in cancer. Dipyridamole (DP) is known as a modifier of the action of cytotoxic drugs. We therefore investigated DP as a potential radiosensitizer and inhibitor of PLD repair in X-irradiated Chinese hamster ovary (CHO) cells in vitro. Exposure to the drug alone resulted in a slight reduction of the clonogenic capacity of the cells. Preincubation for 18 h with 10 and 20 microM DP in cells subcultured at low density, led to a significant radiosensitization. In confluent density-inhibited cultures, preincubation alone as well as pre- and postincubation with 20 microM DP resulted in a significant inhibition of PLD repair. Dipyridamole and related compounds may thus be useful tools for modifying and investigating the response of mammalian cells to radiation.

Animals↗

PubMed1987

Polymeric inhibitors of platelet aggregation. II. Copolymers of dipyridamole and related drugs with N-vinylpyrrolidone.

A study has been made of the behaviour of the drugs dipyridamole and mopidamol (RA 233) attached to poly(N-vinylpyrrolidone). The inhibitory activities towards platelet aggregation induced by ADP or platelet activation factor (PAF) in sheep plasma have been examined and found to exceed the activities of the parent drugs, by factors up to 20. At the same time the abilities of the polymer-bound drugs in potentiating prostaglandin-type anti-aggregatory activities are much lower than those of the unattached drugs. The observations are explained in terms of polymer adsorption on to the platelet membranes, producing a high surface concentration of the drugs with consequent high inhibitory action. Intracellular action, such as the inhibition of phosphodiesterase, is reduced by the difficulty experienced by the polymeric drug in passing through the membrane, so that potentiation of prostaglandin activity, particularly against PAF, becomes small. A terpolymer containing units of dipyridamole and the prostaglandin analogue 5-(6-carboxyhexyl)-1-(3-cyclohexyl-3-hydroxypropyl)hydantoin (245C) shows a degree of 'self-potentiation'.

Adenosine Diphosphate↗

PubMed1992

Interaction of dipyridamole with micelles of lysophosphatidylcholine and with bovine serum albumin: fluorescence studies.

The interaction of the coronary vasodilator dipyridamole with biological systems, protein and membranes has been studied through optical absorption and fluorescence spectroscopies. Using the analysis of the spectra and fluorescence intensity of dipyridamole (DIP) in solution, the interaction of this compound with the transport protein albumin (BSA) and with a model of cell membranes, namely micelles of lysophosphatidylcholine (L-PC), was investigated. Measurements were performed at pH 5.0 and pH 7.0 where the molecule of DIP is fully protonated and partially protonated, respectively. The quenching of fluorescence with nitroxide-stable radicals 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) and 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL) as well as with acrylamide and iodide allowed the localization of the drug in the polar interface of micelles. Quenching by acrylamide and iodide in L-PC micelles demonstrated the effect of micelle protonation which increased the accessibility of iodide to the chromophore. An effective association constant was obtained both at pH 7.0 (7.5 x 10(3) M-1) and pH 5.0 (2.5 x 10(3) M-1) and a very good agreement with the proposed binding model was observed. The quantum yields of fluorescence data agree very well with the fluorescence lifetimes. The measurement of lifetimes was important to understand the kinetic data obtained from Stern-Volmer plots both of radical, acrylamide and iodide quenching of fluorescence. It was observed that, in the presence of micelles, the kq value increased for TEMPO while decreased for TEMPOL. This result, together with the vanishing solubility of DIP in saturated hydrocarbons and the preferential partition of TEMPO in micelles, suggested the localization of DIP in the polar micellar interface. This is also supported by the enhanced iodide quenching at pH 5.0, constancy of acrylamide quenching in the range of pH 7.0-5.0 and the partition of TEMPO and TEMPOL in SDS micelles. The association constant of DIP to BSA was also estimated both at pH 7.0 (2 x 10(4) M-1) and pH 5.0 (4 x 10(3) M-1). Quenching studies with nitroxide radicals, acrylamide and iodide also suggested the binding of the drug to a hydrophobic region of the protein. At pH 5.0, the protein undergo a conformational change which leads to a loosening of the overall structure so that the accessibility of the nitroxide radicals for DIP is increased at this pH. The differences in kq values at pH 7.0 and pH 5.0 suggested that at pH 7.0 the chromophore is protected in the protein site.(ABSTRACT TRUNCATED AT 400 WORDS)

Dipyridamole↗

PubMed1991

Does the association dipyridamole-aspirin only act by a functional synergism?

1. Some of the antiplatelet effects of the dipyridamole-aspirin association may be explained by a functional (additive) synergism, but other effects by a potentiation synergism. 2. Platelet adhesivity and aggregation induced by ADP, adrenaline and collagen, and malondialdehyde production, are tests in which dipyridamole and aspirin shows a potentiation synergism.

Aspirin↗

PubMed1989

Effects of cryptolepine alone and in combination with dipyridamole on a mouse model of arterial thrombosis.

The effects of cryptolepine alone and in combination with other antiplatelet agents have been investigated using a mouse model of arterial thrombosis. Intraperitoneal premedication with crytolepine produced 25% maximal protection at 1 mg/kg while dipyridamole producedd a 20% maximal effect at 2 mg/kg. Higher doses of cryptolepine showed a reduced effect. In contrast, indomethacin and aspirin produced a dose-related and higher degree of protection. A combination of cryptolepine and dipyridamole was more effective than when the individual drugs were used alone. The use of 20% ethanol as a dosage vehicle enhanced the protective effects of all drugs tested and the ethanol vehicle alone provided 45% protection.

Adrenergic alpha-Antagonists↗

PubMed1989

Prognostic importance of silent myocardial ischemia detected by intravenous dipyridamole thallium myocardial imaging in asymptomatic patients with coronary artery disease.

One hundred seven asymptomatic patients who underwent intravenous dipyridamole thallium imaging were evaluated to determine prognostic indicators of subsequent cardiac events over an average follow-up period of 14 +/- 10 months. Univariate analysis of 18 clinical, scintigraphic and angiographic variables revealed that a reversible thallium defect, a combined fixed and reversible thallium defect, number of segmental thallium defects and extent of coronary artery disease were significant predictors of subsequent cardiac events. Of the 13 patients who died or had a nonfatal infarction, 12 had a reversible thallium defect. Stepwise logistic regression analysis selected a reversible thallium defect as the only significant predictor of cardiac events. When death or myocardial infarction was the outcome variable, a combined fixed and reversible thallium defect was the only predictor of outcome. In patients without previous myocardial infarction, the cardiac event rate was significantly greater in those with an abnormal versus normal thallium scan (55% versus 12%, p less than 0.001). Thus, intravenous dipyridamole thallium scintigraphy is a useful noninvasive test to risk stratify asymptomatic patients with coronary artery disease. A reversible thallium defect most likely indicates silent myocardial ischemia in a sizable fraction of patients in this clinical subset and is associated with an unfavorable prognosis.

Aged↗

PubMed1995

Independent prognostic value of intravenous dipyridamole with technetium-99m sestamibi tomographic imaging in predicting cardiac events and cardiac-related hospital admissions.

OBJECTIVES: This study sought to establish the prognostic value of intravenous dipyridamole technetium-99m (Tc-99m) sestamibi single-photon emission computed tomographic (SPECT) myocardial perfusion imaging. BACKGROUND: Optimal management of patients with coronary artery disease involves strategies designed to reduce the risk of myocardial infarction and cardiac death. The role of myocardial perfusion imaging using newer clinical techniques to determine risk and possible benefit from therapy has not been evaluated. METHODS: Myocardial imaging results were classified as normal or abnormal (fixed or reversible defects; small, moderate or large). Follow-up evaluation of all patients included the occurrence of cardiac death or nonfatal myocardial infarction and other cardiac-related hospital admissions. RESULTS: During a mean (+/- SD) follow-up period of 12.8 +/- 6.8 months in 512 patients, 25 had a cardiac event. Patients with abnormal perfusion had significantly more cardiac events than those with normal perfusion (22 vs. 3, p < 0.01). Patients with reversible defects had the highest event rates (8.6%), and those with normal study results had a very low event rate (1.4%). Large defects were strongly associated with more cardiac events and hospital admissions than either normal scan results or abnormal results showing small defects. CONCLUSIONS: Patients with normal study results or a small defect after intravenous dipyridamole Tc-99m sestamibi SPECT imaging had an excellent short-term prognosis. Those with abnormal results (reversible or large defect) had an increased risk of subsequent cardiac death, nonfatal myocardial infarction and other cardiac-related hospital admissions.

Adult↗

PubMed2005

Heart rate response during dipyridamole stress as a predictor of mortality in patients with normal myocardial perfusion and normal electrocardiograms.

Although it is well established that a blunted chronotropic response to exercise is associated with a higher risk of death, recent data suggest a similar association between mortality risk and blunted heart rate response to vasodilatory stress. We investigated the heart rate response to dipyridamole-induced stress as a predictor of death in the setting of normal myocardial perfusion and a normal electrocardiogram. We followed 1,087 patients for 8 years (range 5.7 to 11.8) who underwent dipyridamole vasodilator stress and had normal perfusion scans and electrocardiograms. None had heart failure, known left ventricular systolic dysfunction, pacemaker implantation, or valve disease. Heart rate response was assessed as the ratio of heart rate at peak stress to heart rate at rest. The primary end point was all-cause mortality. Quartile values for the peak-to-rest heart rate ratio were <1.19, 1.19 to 1.30, 1.31 to 1.44, and >1.44. There were 246 deaths. Death rates according to quartiles of heart rate ratio were 103 of 271 (38%), 64 of 272 (24%), 52 of 272 (19%), and 27 of 272 (10%). After adjusting for age, gender, heart rate at rest, blood pressure response, standard cardiovascular risk factors, and other confounders, a blunted heart rate response remained predictive of death (adjusted hazard ratio for lowest vs highest quartile 3.3, 95% confidence interval 2.1 to 5.1, p <0.0001). When considered as a continuous variable, the logarithm of the heart rate ratio was the strongest predictor of death, aside from age. Thus, among patients who have normal myocardial perfusion and normal electrocardiograms, a blunted heart rate response to vasodilator stress is predictive of a marked increase in risk of death.

Aged↗

PubMed2005

Prognostic value of a multiparametric risk score in patients undergoing dipyridamole stress echocardiography.

To set up a prognostic score including clinical data and stress echocardiographic findings, the data of 3,969 patients who underwent dipyridamole stress were analyzed. Age (hazard ratio [HR] 3.21), peak wall motion score index (HR 2.62), diabetes mellitus (HR 2.36), and male gender (HR 1.69) were independent predictors of mortality and were incorporated into a prognostic score allowing us to estimate 1-, 3-, and 5-year survival in the patient cohort. The multiparametric risk score, immediately available at the bedside, can be used to predict the survival of patients undergoing dipyridamole stress echocardiography.

Aged↗

PubMed2006

Electrochemical determination of dipyridamole at a carbon paste electrode using cetyltrimethyl ammonium bromide as enhancing element.

Electrochemical behaviors of dipyridamole (DIP) at a carbon paste electrode in the presence of cetyltrimethyl ammonium bromide (CTAB) were investigated by voltammetry, chronocoulometry and electrochemical impedance spectroscopy (EIS). The results indicated that the electrochemical responses of DIP are apparently improved by CTAB, due to the enhanced accumulation of dipyridamole at the carbon paste electrode surface. Electrochemical parameters for the oxidation of DIP were explored by chronocoulometry. Under optimal conditions, the oxidation peak current at 0.53 V was proportional to DIP concentration in the range of 0.03-12 microg mL-1, with a detection limit of 0.01 microg mL-1 for 120 s accumulation by different pulse voltammetry (DPV). This method was applied to the determination of DIP in the tablet samples. The results were satisfying compared with that obtained by standardized method of high performance liquid chromatography (HPLC).

Carbon↗

PubMed2004

Identifying patients without favourable long-term outcome among those with medically stabilized unstable angina and a negative dipyridamole stress echocardiogram.

AIMS: Patients with medically stabilized unstable angina and a negative stress echocardiogram have a favourable outcome as a whole. This study sought to identify which subsets of patients are associated with serious events at long-term within this population. METHODS AND RESULTS: We studied and followed-up 128 patients (mean 2.2 +/- 1.3 years) with medically stabilized unstable angina and a negative dipyridamole stress echocardiogram. Cumulative survival rates were 98.2 +/- 1.3%, 96.0 +/- 2.2% and 93.2 +/- 3.2%, at 1, 2 and 4 years, respectively. Freedom from events (death, myocardial infarction, and revascularization) were 98.2 +/- 1.3%, 96.0 +/- 2.2% and 86.3 +/- 6.0%, at 1, 2, and 4 years, respectively. Cumulative mortality rate was higher in men (3.6 +/- 2.5%, 8.5 +/- 4.1%, and 12.2 +/- 5.4% at 1, 2, and 4 years, vs. 0% at the end of the follow-up in women; p = 0.034), and in those with previous myocardial infarction (4.3 +/- 4.3%, 9.1 +/- 6.2%, and 18.2 +/- 2.3% at 1, 2 and 4 years, vs. 1.1 +/- 1.1%, 2.9 +/- 2.1%, and 2.9 +/- 2.1% in those without previous myocardial infarction, respectively; p = 0.047). CONCLUSION: Among patients with medically stabilized unstable angina and a negative dipyridamole stress echocardiogram, male gender and previous myocardial infarction are associated with a non-favourable outcome.

Adult↗