NICOTINE INHIBITS HYPOXIA‐ AND ARACHIDONATE‐INDUCED RELEASE OF PROSTACYCLIN‐LIKE ACTIVITY IN RABBIT HEARTS

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Abstract
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. Perfusion was performed with a solution containing 5% C02 in O2. At regular intervals it was changed to a 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 μg/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. Nicotine (5 × 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. 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.