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.