Coronary flow reactions to arachidonic acid are inhibited by docosahexaenoic acid.
Arachidonic acid (AA) administered to isolated perfused rat hearts produced coronary vasoconstriction followed by vasodilatation due to biotransformation of AA into vasoactive metabolites. The formation of these metabolites may be blocked with ibuprofen or fenclorac. Slow infusions of docosahexaenoic acid (DHx) resulted in an inhibition of the coronary responses to AA. These results indicate that DHx behaves as a modulator of coronary responses elicited by AA metabolites.
D000818:Animals; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors*; D003331:Coronary Vessels / Q000187:drug effects*; D004281:Docosahexaenoic Acids; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D007052:Ibuprofen / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D010648:Phenylacetates / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis; D051381:Rats
D001095:Arachidonic Acids; D005231:Fatty Acids, Unsaturated; D010648:Phenylacetates; D011453:Prostaglandins; D004281:Docosahexaenoic Acids; C013530:fenclorac; D007052:Ibuprofen