Nicotine inhibits hypoxia- and arachidonate-induced release of prostacyclin-like activity in rabbit hearts.
1 Rabbit hearts were perfused by the Langendorff technique and the interstitial effluent content of platelet anti-aggregatory activity (prostacyclin-like activity) was assayed at regular intervals. 2 Perfusion was performed with a solution containing 5% CO2 in O2. At regular intervals it was changed to solution containing 12% O2 and 5% CO2 in N2. Alternatively, perfusion with 5% CO2 in O2 was maintained during the entire experiment and sodium arachidonate was infused (5 to 15 microgram/min) at intervals. Under the basal conditions no efflux of prostacyclin-like activity was observed in the interstitial cardiac effluent, but both perfusion with a hypoxic solution and infusion of arachidonate induced such release. 3 Nicotine (5 X 10(-5) M) in the solution perfusing the heart markedly inhibited the efflux of prostacyclin-like activity into the cardiac interstitial effluent, induced by hypoxia or by infusion of arachidonate. 4 It is suggested that nicotine counteracts the formation of prostacyclin-like activity in the rabbit heart by interfering with the enzymatic conversion of arachidonate to prostacyclin.
D000818:Animals; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis*; D005260:Female; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009538:Nicotine / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000096:biosynthesis*; D011817:Rabbits
D001095:Arachidonic Acids; D011453:Prostaglandins; D009538:Nicotine; D011464:Epoprostenol