Acute effects of intravenous trapidil on hemodynamics, coronary circulation and myocardial metabolism in man.
The acute effects of intravenous trapidil on hemodynamics, coronary circulation and myocardial metabolism were evaluated in 19 patients (Group I: 10 patients of chest pain syndrome; Group II: 9 patients of coronary heart disease). The heart rate increased (p less than 0.05) and aortic pressure decreased (p less than 0.01) during a 6-min study period. Pulmonary arterial end-diastolic pressure decreased slightly in both groups and cardiac output increased prominently in Group II. Myocardial oxygen consumption did not change significantly 3 and 6 min after trapidil injection. Coronary sinus flow increased slightly (statistically not significant) despite a decrease in aortic pressure, and thus, coronary vascular resistance decreased significantly in both groups. Coronary A-V O2 difference decreased 3 min after trapidil injection and no significant change in the lactate extraction ratio was observed. The diameter of the left main coronary artery increased by about 6% after an administration of trapidil. These results suggest that trapidil has the beneficial effect of coronary vasodilation and it increases cardiac output, despite a decrease in the preload, without a significant increase in myocardial oxygen consumption. The latter may be due to an afterload reduction effect of this drug.
D000368:Aged; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007263:Infusions, Parenteral; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D010146:Pain / Q000503:physiopathology; D011743:Pyrimidines / Q000494:pharmacology*; D013909:Thorax; D014192:Trapidil / Q000008:administration & dosage / Q000494:pharmacology*; D014655:Vascular Resistance / Q000187:drug effects
D011743:Pyrimidines; D014192:Trapidil