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NICOTINE INHIBITS HYPOXIA‐ AND ARACHIDONATE‐INDUCED RELEASE OF PROSTACYCLIN‐LIKE ACTIVITY IN RABBIT HEARTS
Author(s) -
WENNMALM ÅKE
Publication year - 1980
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1980.tb07901.x
Subject(s) - prostacyclin , perfusion , chemistry , nicotine , hypoxia (environmental) , medicine , endocrinology , pharmacology , biochemistry , oxygen , organic chemistry
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% C0 2 in O 2 . At regular intervals it was changed to a solution containing 12% O 2 and 5% CO 2 in N 2 . Alternatively, perfusion with 5% CO 2 in O 2 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.