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

Abstract

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% 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. 3 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. 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.