Prostacyclin-dependent coronary vasodilation in rabbit and guinea pig hearts.
Isolated hearts from rabbits or guinea pigs were perfused according to Langendorff and the coronary flow was recorded continuously. In addition, the rabbit heart transmyocardial effluent's content of platelet anti-aggregatory (prostacyclin-like, PCLA) activity was assayed biologically at regular intervals. Perfusion was performed with a solution gassed with 95% O2 in CO2, switching at intervals to a solution gassed with 12% O2 and 5% CO2 in N2. Perfusion with a hypoxic solution elicited reproducible increased in coronary flow. After pretreatment with indomethacin (5 x 10-5M), this increase was completely abolished and in several cases it was reversed to a marked reduction in cornonary flow. The transmyocardial effluent contained, during perfusion with normoxic solution, no detectable or only negligible amounts of PCLA. During hypoxia the efflux of PCAL into the transmyocardial effluent increased markedly. This increase was completely abolished when indomethacin (5 x 10-5M) was added to the solution perfusing the heart. The results strongly suggest that increased coronary vascular formation of prostacyclin plays a key role in the coronary vasodilation induced by hypoxia in rabbit and guinea pig hearts.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D011464:Epoprostenol / Q000096:biosynthesis / Q000502:physiology*; D005260:Female; D006321:Heart / Q000502:physiology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000502:physiology*; D011817:Rabbits; D014664:Vasodilation / Q000187:drug effects
D011453:Prostaglandins; D000244:Adenosine Diphosphate; D011464:Epoprostenol; D007213:Indomethacin