Myocardial biosynthesis of prostaglandins with special consideration of prostacyclin and the influence of dipyridamole and propranolol.
Experiments with isolated perfused hearts of guinea pigs and rats showed that cardiac action is linked to formation of prostaglandinlike substances (PLS) and prostacyclin (PGI2). Perfusion of the hearts with arachidonic acid or pretreatment with a linoleic-acid-supplemented diet significantly increased the content of PLS and PGI2 and exerted an economic effect on the heart performance. Dipyridamole induced a marked increase in the coronary flow and PGI2 formation of the hearts but decreased the enhanced myocardial PGI2 biosynthesis after perfusion with arachidonic acid. Propranolol also caused a rise in PGI2 efflux but did not show any influence on PGI2 formation after arachidonic acid. Dipyridamole and propranolol prevent decreased PGI2 formation after acetylsalicylic acid, supporting the view that a combination of these drugs exerts a preventive effect in patients with angina pectoris and heart infarction.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology*; D004176:Dipyridamole / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis*; D006168:Guinea Pigs; D006339:Heart Rate / Q000187:drug effects; D008041:Linoleic Acids / Q000494:pharmacology*; D009206:Myocardium / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats
D001095:Arachidonic Acids; D008041:Linoleic Acids; D011453:Prostaglandins; D004176:Dipyridamole; D011433:Propranolol; D011464:Epoprostenol