Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIPYRIDAMOLE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1993

Evaluation of coronary artery disease extent using 99Tcm-sestamibi: comparison of dipyridamole versus exercise and of planar versus tomographic imaging.

The aim of this study was to compare the reliability of 99Tcm-sestamibi myocardial scintigraphy for the assessment of coronary artery disease extent using two different stresses (exercise and dipyridamole) and imaging techniques (planar versus single photon emission tomography, SPET) in a patient population of 20 subjects, all also studied with coronary angiography. The agreement of exercise and dipyridamole was good for the visual uptake score (planar kappa = 0.71, SPET kappa = 0.64) and for abnormal segment detection (planar and SPET both kappa = 0.76). For the recognition of the individual diseased vessel, the results of exercise and dipyridamole planar scans were equal (sensitivity 49%, specificity 90%, accuracy 63%); those of exercise and dipyridamole SPET were also similar and were both better than the related planar data (sensitivity 79% and 74%, P < 0.005 and < 0.02, respectively, versus planar; specificity 95% and 100%; accuracy 85 and 83%, P < 0.001 and < 0.02 versus planar). Both stresses and imaging techniques were less sensitive in cases of mild (50 to 70%) obstructions. In conclusion, exercise and dipyridamole appear equally effective stresses for 99Tcm-sestamibi scintigraphy; with both of them, however, SPET allows significantly better results than planar imaging and therefore should be recommended.

Adult↗
PubMed2002

Long-term prognostic value of dipyridamole echocardiography in vascular surgery: a large-scale multicenter study.

BACKGROUND: Late cardiac events after non-cardiac major vascular surgery are an important cause of morbidity and mortality. The aim of the present study was to assess the value of a preoperative dipyridamole echocardiography test (up to 0.84 mg/kg over 10 min) in predicting late cardiac events in survivors of major non-cardiac vascular surgery. DESIGN: Large-scale, multicenter, prospective, observational study design. METHODS: Two hundred and seventy-six patients (mean age 66 +/- 9 years) were studied prior to vascular surgery by dipyridamole stress echocardiography in four different centres. All patients underwent preoperative clinical risk assessment according to the American Heart Association guidelines. All underwent dipyridamole stress echocardiography according to standard high-dose protocol. RESULTS: No major complications occurred during dipyridamole stress echocardiography. Sixty-three patients (23%) had a positive test. Patients were followed up for a median of 20 months. Cardiac events occurred in 43 patients (16%): five deaths, 18 myocardial infarctions and 20 cases of unstable angina. The difference between wall-motion score index (WMSI) at rest and peak stress (delta WMSI), using multivariate analysis, was an independent predictor of late cardiac death. CONCLUSION: Dipyridamole stress echocardiography performed before major vascular surgery identifies patients at high risk for late cardiac events. Stress echocardiographic parameters outperformed clinical variables in the long-term risk stratification in this set of patients.

Aged↗
PubMed2003

Reactive hyperemia following coronary balloon angioplasty, but not dipyridamole-induced hyperemia, predicts resolution of exercise-induced ST-segment depression.

OBJECTIVES: To characterize delayed restoration of coronary blood flow following successful percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Delayed restoration of coronary blood flow following successful PTCA is common and likely the result of multiple factors. Temporary myocardial ischemia and dipyridamole administration both result in increased coronary blood flow, but by different mechanisms. The relationship between these phenomena and exercise-induced ST-segment depression after PTCA was investigated to determine if any correlation existed. METHODS: Forty consecutive patients with single-vessel coronary artery disease underwent treadmill exercise testing before and after PTCA. The percentage change in coronary blood flow before and after 90 s balloon inflation was assessed. After a new steady state had been reached, dipyridamole was infused and changes in coronary blood flow were again determined. The relationship between changes in coronary blood flow and the presence of ST-segment depression during exercise testing after PTCA was determined. RESULTS: Peak coronary blood flow induced by reactive hyperemia was significantly greater than that in the steady state after balloon inflation (48.5+/-38.8 compared with 15.1+/-13.2 ml/min, P<0.0001). Dipyridamole administration also resulted in significant increases in coronary blood flow (15.1+/-13.2 ml/min compared with 31.0+/-24.9 ml/min, P<0.0001). ST-segment depression after PTCA was significantly less than before (0.10+/-0.07 mV compared with 0.19+/-0.08 mV, P<0.001). Further, reactive hyperemia, but not dipyridamole-induced hyperemia, correlated with attenuation of exercise-induced ST-segment depression after PTCA (r=0.62, P<0.0001). CONCLUSIONS: Reactive hyperemia following temporary coronary occlusion recreates local conditions associated with delayed resolution of myocardial ischemia following successful PTCA. Further, this phenomenon appears to be distinct from changes in coronary blood flow induced by dipyridamole.

Adult↗
PubMed1985

Pharmacokinetic interaction of acetylsalicylic acid and dipyridamole.

It is often recommended that acetylsalicylic acid (ASA) and dipyridamole should be given together in order to obtain secondary prophylaxis against certain ischaemic diseases. Therefore, the possible pharmacokinetic interactions between these agents were assessed following single-dose exposures in 14 healthy volunteers. The plasma concentrations of ASA, salicylic acid (SA) and dipyridamole were measured by selective h.p.l.c. techniques. It was found that, while dipyridamole kinetics were unaffected by concurrent ASA, concurrent dipyridamole significantly enhanced the peak concentration (24%) and AUC (27%) of ASA. Thus, co-administered dipyridamole might influence the anti-platelet effect of ASA.

Adult↗
PubMed2003

Blunted increase in plasma adenosine levels following dipyridamole stress in dilated cardiomyopathy patients.

BACKGROUND: Heart failure is characterized by chronically increased adenosine levels, which are thought to express a protective anti-heart failure activation of the adenosinergic system. The aim of the study was to assess whether the activation of adenosinergic system in idiopathic dilated cardiomyopathy (IDC) can be mirrored by a blunted increase in plasma adenosine concentration following dipyridamole stress, which accumulates endogenous adenosine. METHODS: Two groups were studied: IDC patients (n = 19, seven women, mean age 60 +/- 12 years) with angiographically confirmed normal coronary arteries and left ventricular ejection fraction <35%; and normal controls (n = 15, six women, mean age 68 +/- 5 years). Plasma adenosine was assessed by high-performance liquid chromatography methods in blood samples from peripheral vein at baseline and 12 min after dipyridamole infusion (0.84 mg kg-1 in 10 min). RESULTS: At baseline, IDC patients showed higher plasma adenosine levels than controls (276 +/- 27 nM L-1 vs. 208 +/- 48 nM L-1, P < 0.001). Following dipyridamole, IDC patients showed lower plasma adenosine levels than controls (322 +/- 56 nM L-1 vs. 732 +/- 250 nM L-1, P < 0.001). The dipyridamole-induced percentage increase in plasma adenosine over baseline was 17% in IDC and 251% in controls (P < 0.001). By individual patient analysis, 18 IDC patients exceeded (over the upper limit) the 95% confidence limits for normal plasma adenosine levels at baseline, and all 19 exceeded (below the lower limit) the 95% confidence limits for postdipyridamole plasma adenosine levels found in normal subjects. CONCLUSION: Patients with IDC have abnormally high baseline adenosine levels and--even more strikingly--blunted plasma adenosine increase following dipyridamole infusion. This is consistent with a chronic activation of the adenosinergic system present in IDC, which can be measured noninvasively in the clinical theatre.

Adenosine↗
PubMed2004

Arterial concentration of 99mTc-sestamibi at rest, during peak exercise and after dipyridamole infusion.

Tracers for myocardial perfusion imaging during stress should not only have high cardiac uptake but they should also have a fast blood clearance to prevent myocardial tracer uptake after the ischaemic stimulus. The present study characterize the early phase of the arterial (99m)Tc-sestamibi (MIBI) time-activity curve after venous bolus injection at rest, during peak exercise and after dipyridamole infusion. We included 11 patients undergoing angioplasty for one-vessel disease (rest study) and 20 patients evaluated for the detection of haemodynamic significant coronary stenoses by (99m)Tc-sestamibi single photon emission computed tomography (SPECT) using either bicycle exercise testing (10 patients) or standard dipyridamole testing (10 patients). Arterial blood samples of 1 ml were taken from the left femoral artery (rest study) or the right radial artery (exercise and dipyridamole studies) every 5 s during the first 5 min postinjection. In the exercise and the dipyridamole studies blood sampling were extended to include blood samples every 5 min 5-30 min postinjection. Peak MIBI concentration was lower and decrease in concentration slower after tracer injection during exercise than during dipyridamole stress testing. This may cause an underestimation of perfusion defects during exercise because of MIBI uptake after the ischaemic stimulus. The implications of the study not only refer to the choice of stress modality when using MIBI. This study also underlines the importance of considering early blood clearance in addition to regional myocardial tracerkinetic aspects such as myocardial extraction fraction when new tracers are introduced.

Arteries↗
PubMed1975

Adenosine and dipyridamole actions and interactions on isolated coronary artery strips of cattle.

1 The actions and interactions of adenosine and dipyridamole were investigated on isolated strips of coronary arteries of beef cattle. It was found that small diameter arteries (about 0.5-1.0 mm o9d.), raised to a moderate level of tone with potassium, responded with relaxation to low concentrations of adenosine. 2 Dipyridamole, over a broad concentration range (6.0 X 10(-8)-2.0 X 10(-5)M), enhanced these responses, shifting the adenosine concentration-response curve (3.7 X 10(-8)-1.1 X 10(-4)M) considerably to the left. In contrast, inhibitory concentrations-response curves to sodium nitrite and to noradrenaline were not materially altered by dipyridamole. 3 Studies of the uptake of [3H]-adenosine revealed a rapid uptake of the nucleoside by coronary artery strips, which was inhibited by dipyridamole (6.0X 10(-8)-2.0X10(-5)M); but this may not be sufficient to account fully for the observed sensitization. 4 It is concluded that the regulation of adenosine responses and the action of dipyridamole in the heart involve a more direct association with coronary vascular tissue than has been previously appreciated.

Adenosine↗
PubMed1981

Effect of various doses of acetylsalicylic acid in combination with dipyridamole on the balance between prostacyclin and thromboxane in human serum.

1 Thirty-six healthy human subjects were randomly divided into six groups which were treated with a single dose of 75 mg (1.3 mg/kg) of dipyridamole alone, or 75 mg of dipyridamole in combination with 30 mg (0.5 mg/kg), 50 mg (0.8 mg/kg), 160 mg (2.6 mg/kg) and 330 mg (5.7 mg/kg) of acetylsalicylic acid (ASA), or with placebo. 2 The concentrations of prostacyclin (PGI2) and thromboxane A2 (TxA2) metabolites, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and TxB2 respectively, were measured in serum with specific radioimmunoassays before and 1 and 3 h afer the ingestion of the test dose. 3 The basal concentrations of 6-keto-PGF1 alpha and TxB2 correlated significantly (r = 0.588, P less than 0.001). 4 Dipyridamole alone did not change PGI2 or TxA2 production. 5 Dipyridamole-ASA combinations with ASA doses between 0.5 and 0.8 mg/kg inhibited TxB2 production by 48 to 74% and with the ASA doses between 2.6 and 5.7 mg/kg by about 90%. None of these combinations changed PGI2 production. 6 The ratio of 6-keto-PGF1 alpha to TxB2 increased 3.5 to 6 times with ASA doses of 0.5 to 0.8 mg/kg and 21 to 29 times with doses between 2.6 to 5.7 mg/kg. 7 These results suggest that the anti-thrombotic effect of dipyridamole in vivo is not mediated through direct changes in PGI2 and/or TxA2 production.

Adult↗
PubMed1998

Noninvasive diagnosis of gastroesophageal inflammation using dipyridamole thallium-201 tomography.

OBJECTIVE: Esophagitis, a complication of GERD, and gastric erosions are common findings in dyspeptic patients. Unfortunately, these findings cannot be predicted based on symptoms alone and require endoscopy for an accurate diagnosis. Noninvasive diagnosis of other gastrointestinal pathology by radiopharmaceuticals (GA 67, Tc 99m pertechnetate) has previously been studied. We hypothesized that endoscopically documented esophagitis and/or gastric erosions could also be detected by using dipyridamole thallium-201 imaging and, if they were of sufficient accuracy, could serve as a useful, noninvasive screening test for esophagitis and/or gastric erosions. METHODS: A pilot study was undertaken in 12 patients undergoing endoscopy for symptoms of GERD or dyspepsia. Esophagitis was defined as the presence of either erosions or ulceration and gastric erosions were defined as discrete mucosal breaks measuring > or = 1 mm. Dipyridamole thallium-201 imaging was performed the following day on all 12 patients. A standard dose of dipyridamole (0.56 mg/kg) was infused over 4 min, followed by a 3-mCi dose of thallium-201. Initial stress tomographic images and reinjection (1 mCi) resting tomographic images 3-4 h later were obtained using a gamma camera. Tomographic images were read blinded to the endoscopy results. Thallium-201 uptake was graded on a 0-3+ scale using the liver uptake as the internal comparative standard (2+ = uptake equal to the liver). Abnormal thallium uptake was defined as > or = 2+ in the area of the esophagus or stomach. RESULTS: Seven women and five men (mean age 41 yr, range 25-60 yr) were studied. Eight patients were taking histamine-2 receptor antagonists and none were on proton pump inhibitors, or promotility agents. All five patients with endoscopic esophagitis had a positive thallium-201 tomographic image. Seven patients had no evidence of esophagitis, and three had positive thallium-201 tomograms. Dipyridamole thallium-201 imaging sensitivity, specificity, and positive and negative predictive values for esophagitis were 100%, 57%, 63%, and 100%, respectively. All three patients with gastric erosions had positive thallium-201 tomograms. Six of nine patients without gastric erosions had positive tomograms. The sensitivity, specificity, and positive and negative predictive values of DT 201 gastric erosions were 100%, 33%, 33%, and 100%, respectively. CONCLUSIONS: Dipyridamole thallium-201 tomographic imaging has good sensitivity (100%) in detecting esophagogastric mucosal erosions, but its poor specificity (33-57%) results in an unacceptable accuracy as a screening test. Additionally, the cost of radiopharmaceuticals requires that sensitivity and specificity be at least equal to that of endoscopy for this test to be clinically valuable as a screening test. However, a noninvasive test for these diseases is inherently appealing, and further research in this area seems to be warranted.

Adult↗
PubMed1987

Cardiovascular effects of infused adenosine in man: potentiation by dipyridamole.

In a single blind randomized study, eight normal subjects (23-40 years) received on two separate days adenosine as a constant i.v. infusion with doses increasing from 0.005-0.1 mg kg-1 min-1 following either i.v. dipyridamole 0.4 mg kg-1 per 10 min or a corresponding volume of saline. Heart rate, blood pressure and skin temperature were measured. Following saline all subjects tolerated adenosine 0.07 mg kg-1 min-1, six also tolerated 0.09 mg kg-1 min-1. Both heart rate and skin temperature increased with adenosine in a dose-related manner. Thus, adenosine 0.09 mg kg-1 min-1 was associated with an increase in heart rate (mean +/- SD) from baseline before saline with 16 +/- 10 b.p.m. (P less than 0.01) and an increase in skin temperature with 1.3 +/- 0.8 degrees C (P less than 0.02). Dipyridamole, which inhibits the cellular uptake of adenosine was associated with a change in heart rate similar to that induced by adenosine. Furthermore, when adenosine was infused following dipyridamole the changes in heart rate and skin temperature were potentiated as compared with adenosine following saline. Thus, following dipyridamole an increase in heart rate with 15 b.p.m. above baseline was obtained with 0.005 mg kg-1 min-1 of adenosine as compared with 0.08-0.09 mg kg-1 min-1 of adenosine following saline. Blood pressure did not change in any of the studies. Exogenous adenosine in man has a dose-related positive chronotropic effect and a local dilatory effect in the skin microcirculation. Dipyridamole potentiates the cardiovascular effects of infused adenosine in man.

Adenosine↗
PubMed1988

Short term reproducibility of exercise testing in patients with ST segment elevation and different responses to the dipyridamole test.

The short term reproducibility of exercise testing in 25 patients who had exercise induced ST segment elevation without baseline regional asynergy or a previous myocardial infarction, who had different responses to the dipyridamole test, was assessed. The patients performed a dipyridamole echocardiography test and a second exercise stress test. All underwent coronary arteriography. Seventeen patients had transient regional asynergy after dipyridamole (group 1) and either ST segment elevation (14 patients) or depression (three patients); a second group of eight had no asynergy and no electrocardiographic changes (group 2). The repeated exercise stress test was positive in 16 of the 17 patients of group 1 (11 with ST elevation and five with ST depression) and in two patients of group 2 (both had ST depression and one had coronary artery disease). The dipyridamole echocardiography test was positive in 17 of the 19 patients with coronary artery disease and was negative in all six patients without coronary artery disease. The repeated exercise stress test was positive in 17 of the 19 patients with coronary artery disease and in one patient without. The dipyridamole echocardiography test and a repeated exercise stress test, but not a single exercise stress test, identified coronary artery disease causing exercise induced ST segment elevation.

Adult↗
PubMed1991

Characteristics of left ventricular filling in coronary artery disease and myocardial ischaemia after dipyridamole provocation.

Doppler echocardiographic measurement of transmitral filling velocities seems to be a sensitive marker for resting left ventricular diastolic abnormalities in patients with coronary artery disease. The behaviour of these filling velocities during induced myocardial ischaemia, however, has not been fully studied. Left ventricular filling was assessed by pulsed Doppler ultrasound in 21 patients with angina pectoris and coronary artery disease and in five controls (patients with chest pain but without myocardial ischaemia). High dose dipyridamole infusion (0.9 mg/kg over 10 minutes) was used to provoke myocardial ischaemia, which was assessed by symptoms and electrocardiographic ST segment change. Doppler indices of diastolic filling were measured and the results expressed as percentage change from baseline values. Dipyridamole increased the heart rate and reduced systolic blood pressure equally in both groups. In the controls dipyridamole increased the peak filling velocities of both the early and atrial filling waves. In the 12 patients with coronary artery disease who did not develop evidence of myocardial ischaemia, the effect on left ventricular filling velocity resembled that in the controls though the time to peak change was delayed. Six of the nine patients with dipyridamole induced myocardial ischaemia had a significantly reduced maximum changes in early (+30% v +18%) and atrial (-0.2% v +33%) filling velocities compared with the controls. The remaining three patients had a decrease in early filling velocity (-20%) with an associated increase in atrial peak filling velocity (+21%). Dipyridamole increased diastolic filling velocities in the controls. In patients with coronary artery disease there was a variable change in diastolic filling indices which may be attributed either to the degree of myocardial ischaemia or to the different haemodynamic changes occurring during myocardial ischaemia.

Adult↗
PubMed1996

Comparison of dobutamine stress echocardiography with dipyridamole stress echocardiography for detection of viable myocardium after myocardial infarction treated with thrombolysis.

OBJECTIVE: To compare the ability of dobutamine and dipyridamole stress echocardiography to detect functional recovery of stunned but viable myocardial regions early after acute myocardial infarction, and to predict late functional recovery of the reperfusion salvaged myocardium within the infarct area. METHODS: Within 10 d of acute myocardial infarction, 51 patients--30 anterior and 21 inferior, 44 Q wave and seven non-Q-wave infarction--were submitted to a dobutamine echocardiography test at low dose (5-10 micrograms/kg/min over 5 min) and high dose (20-40 micrograms/kg/min over 3 min) and to dipyridamole echocardiography test (0.56 mg/kg over 4 min + 0.28 mg/kg over 2 min) on different days and in random order, after interruption of any vasoactive drug. Resting echocardiography was repeated at two months in 41 of 51 patients (80%). Regional wall motion of the left ventricle was analysed in a semiquantitative manner on a 14-segment model. Viability was defined as improvement of one grade or more of at least two basally asynergic segments in the infarcted area. RESULTS: Regional functional recovery was detected by low dose dobutamine in 38/51 patients (75%) and in 147/308 (48%) of basally asynergic segments, compared to 25/51 patients (49%; P < 0.001) and 78/308 segments (25%; P < 0.001) only identified by dipyridamole. Late spontaneous functional recovery was detected in 24/41 patients (59%) and in 78/254 basally asynergic segments (31%). The sensitivity of dobutamine and dipyridamole echocardiography for predicting spontaneous functional recovery was 72% and 51% respectively (P < 0.001), specificity 68% and 82% (P < 0.001), positive predictive value 50% and 56%, and negative predictive value 85% and 79%. CONCLUSIONS: In comparison with dipyridamole in patients with thrombolysed myocardial infarction, dobutamine induces regional functional recovery. This suggests that dobutamine is more sensitive in showing the presence of viable myocardium within the infarct zone, though it has a lower specificity in predicting delayed spontaneous functional recovery of non-contractile but still viable areas.

Coronary Angiography↗
PubMed1996

Mechanisms of regional ischaemic changes during dipyridamole echocardiography in patients with severe aortic valve stenosis and normal coronary arteries.

OBJECTIVE: Vasodilator stress echocardiography can cause myocardial ischaemia in patients with severe aortic valve stenosis and angiographically normal coronary arteries. The aim of the study was to determine the mechanism of ischaemia in this clinical model. METHODS: The study group comprised patients with severe aortic valve stenosis and normal coronary arteries: 25 patients (17 males, eight females; age 63 (SD 11) years) underwent a high dose (up to 0.84 mg/kg over 10 min) dipyridamole echocardiography test both before (2-4 d) and after (10-15 d) aortic valve replacement. Mean aortic pressure gradient was 96 (15) mm Hg, with a left ventricular mass index of 228 (49) g/m2. The dipyridamole echocardiography test was well tolerated and interpretable in all patients. RESULTS: Dipyridamole infusion induced chest pain in seven patients before and in no patient after surgery (28 v 0%, P < 0.01), ST segment depression in 12 patients before and two after surgery (48 v 8%, P < 0.01), and a transient regional dyssynergy in 10 patients before and two after surgery (40 v 8%, P < 0.01). In the preoperative evaluation, patients with an echocardiographically positive dipyridamole echocardiography test were comparable with patients with negative test as far as left ventricular mass index [240 (67) v 230 (64) g/m2, NS] and mean aortic pressure gradient [95 (22) v 92 (21) mm Hg, NS] were concerned. When compared to the preoperative assessment, the resting echo assessment in the postoperative evaluation showed unchanged values of left ventricular mass index [pre 228 (49) g/m2 v post 220 (36) g/m2, NS], but markedly decreased values of mean aortic gradient [pre 95 (15) mm Hg v post 22 (5) mm Hg, P < 0.01] and left ventricular wall stress index [pre 134 (30) g/cm2 v post 89 (19) g/cm2]. CONCLUSIONS: Dipyridamole echocardiography is a suitable clinical technique for assessing the ischaemic vulnerability of the left ventricle in severe aortic valve stenosis with angiographically normal coronary arteries. The frequent disappearance of the ischaemic response early after aortic valve replacement suggests that haemodynamic factors such as compressive diastolic wall stress or afterload reduction are important components of myocardial ischaemic vulnerability under these circumstances.

Adult↗
PubMed1977

Inhibition of hypoxic pulmonary vasoconstriction by dipyridamole is not platelet mediated.

Dipyridamole, which is known to alter platelet function, has also been shown to reduce hypoxic pulmonary vasoconstriction. This latter effect could result from dipyridamole either acting on a platelet-mediated system, or acting directly on pulmonary vascular smooth muscle. To investigate these two possibilities, normal dogs were compared with dogs rendered thrombocytopenic by a platelet antiserum. Compared with the hypoxic pressor response before drug treatment, the hypoxic response following dipyridamole was only 32% as great in the normal dogs and only 38% as great in the thrombocytopenic dogs. Thus, dipyridamole was no less effective in reducing the hypoxic pressor response in the virtual absence of platelets. This supports a direct effect of dipyridamole on pulmonary vascular smooth muscle, which could be mediated by an increase in adenosine levels.

Animals↗
PubMed1986

Conditions for dipyridamole potentiation of skeletal muscle active hyperemia.

The effects of dipyridamole on active hyperemia were evaluated in dog gracilis muscles undergoing sustained isometric contractions. Muscles were stimulated to contract for 5, 15, 25, and 50 s at 20% maximal tension (20% Tmax) or for 10 s at 100% Tmax during intra-arterial infusion of either saline or dipyridamole (1 microM). In two separate groups of dogs, muscles were stimulated to contract under free-flow or restricted-flow (ischemic) conditions. In the later group, blood flow was reduced to 50% of precontraction level during the period of contraction. Dipyridamole increased resting vascular conductance by about 45%; however, it did not affect the change in vascular conductance resulting from muscle contraction. The recovery time for active hyperemia following free-flow contractions at 20% Tmax was not altered by dipyridamole. However, dipyridamole increased the recovery time following 50 s of restricted-flow contraction (20% Tmax) and 10 s of 100% Tmax contractions by 46 and 169%, respectively. These results suggest that adenosine contributes to active hyperemia following sustained ischemic contractions at 20% Tmax and contractions at 100% Tmax but not from contractions at 20% Tmax where blood flow is allowed to increase freely.

Animals↗
PubMed1989

Redistribution of coronary microvascular resistance produced by dipyridamole.

This study assessed the redistribution of coronary microvascular resistance during vasodilation produced by dipyridamole. Measurements of microvascular diameter and pressure in the beating left ventricle of anesthetized cats were accomplished by means of a computer-controlled system that enabled measurements in the beating heart. Resistances of coronary arteries, microvessels, and veins were calculated from the quotients of the pressure gradient across each vascular compartment and myocardial perfusion (radioactive microspheres). Administration of dipyridamole increased coronary blood flow from 1.80 +/- 0.09 to 6.42 +/- 0.31 ml.min-1. g-1 (P less than 0.05). During control conditions, 25 +/- 8% of total resistance occurred in coronary arteries (proximal to 170 microns), 68 +/- 8% of total resistance was in coronary microvessels (between arterioles less than 170 microns in diameter and venules less than 150 microns in diameter), and 7 +/- 7% of resistance resided in veins (distal to 150 microns). There was a significant redistribution (P less than 0.05) of resistance in all vessel classes after dipyridamole: coronary arteries constituted 42 +/- 6%, microvessels contained 27 +/- 5%, and veins had 31 +/- 8% of total coronary resistance. During control conditions, vascular resistance in coronary arteries and microvessels was 17 +/- 4 and 45 +/- 6 mmHg.min.g.ml-1, respectively. During vasodilation, resistance was significantly reduced (P less than 0.05) in both the arterial and microvessel segments to 6 +/- 2 and 4 +/- 2 mmHg.min.g.ml-1, respectively. Venous resistance was not significantly affected during dipyridamole-induced vasodilation. In conclusion, there was a marked reduction of coronary vascular resistance in response to dipyridamole, with the major component accounted for by dilation of microvessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Effects of dipyridamole and adenosine infusions on ovine pulmonary and systemic circulations.

This study was designed to test the hypothesis that A2 adenosine receptors mediate the hemodynamic responses to intravenous infusions of dipyridamole. We tested the hypothesis using theophylline, which has been reported to block A2 adenosine receptors and thereby attenuate the vasodilation caused by adenosine. Twenty-four anesthetized lambs that were between 7 and 17 days of age were used. Basal vascular tone of each animal was increased with the thromboxane mimetic U-46619. A theophylline dose commonly used in humans (5.0 mg/kg infused over 30 min followed by 1.0 mg x kg(-1) x h(-1)) resulted in negligible changes in the vasodilation caused by either dipyridamole or adenosine. However, a 10-fold greater theophylline dose significantly attenuated the vasodilation caused by adenosine, yet the attenuation in vasodilation caused by dipyridamole remained negligible. In addition, dipyridamole caused a weakly preferential pulmonary vasodilation, whereas adenosine caused a strongly preferential systemic vasodilation. These findings suggest that dipyridamole dilates effectively both the pulmonary vasculature and the systemic vasculature via predominantly adenosine-independent mechanisms.

Adenosine↗