The effects of dipyridamole on coronary post-occlusion hyperaemia and on myocardial vasodilatation induced by systemic hypoxia.
1. The arterial pO(2) of anaesthetized cats was reduced to 33 mmHg by supplying a mixture of oxygen and nitrogen as the respiratory gas. This produced vasodilatation in the myocardial bed which was not increased after the injection of dipyridamole (1 mg/kg).2. Reactive hyperaemia was observed following occlusion of the left anterior descending coronary artery for 10-120 seconds. The duration of the period of reactive hyperaemia was increased after the injection of dipyridamole. This effect of dipyridamole was most pronounced when the longest periods of occlusion were used.3. These results support the hypothesis that myocardial reactive hyperaemia is at least partly caused by adenosine released from hypoxic myocardial cells. The vasodilatation occurring during systemic hypoxia, on the other hand, is probably mediated via a different mechanism.
D000818:Animals; D001565:Benzoates / Q000494:pharmacology; D001794:Blood Pressure; D002404:Catheterization; D002415:Cats; D003331:Coronary Vessels / Q000187:drug effects*; D004176:Dipyridamole / Q000494:pharmacology*; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000187:drug effects; D006333:Heart Failure / Q000503:physiopathology*; D006940:Hyperemia; D000860:Hypoxia / Q000503:physiopathology*; D008026:Ligation; D008297:Male; D010100:Oxygen / Q000097:blood; D014655:Vascular Resistance
D001565:Benzoates; D004176:Dipyridamole; D010100:Oxygen