对乙酰氨基酚或花生四烯酸诱导的离体大鼠心脏冠状动脉舒张及前列腺素释放的抑制作用。

Attenuation by acetaminophen or arachidonic acid-induced coronary vasodilation and output of prostaglandins in the isolated rat heart.

作者信息

Shaffer J E, Cagen L M, Malik K U

出版信息

Eur J Pharmacol. 1981 Jun 10;72(1):57-61. doi: 10.1016/0014-2999(81)90296-x.

Abstract

We studied the effect of acetaminophen on the vascular actions of arachidonic acid and on the output of prostaglandins in the isolated rat heart. Arachidonic acid (33 nmol), administered as a bolus into the heart through the aortic cannula produced vasoconstriction followed by a long lasting vasodilation. Arachidonic acid also markedly increased the output of PGE2 and 6-keto-PGF1 alpha from the heart. In the presence of acetaminophen (0.1-1.0 mM) both the output of prostaglandins and the duration of the coronary vasodilation were attenuated. We suggest that the major component of arachidonic acid-induced coronary vasodilation is mediated through prostaglandin synthesis and is blocked by acetaminophen.

摘要

我们研究了对乙酰氨基酚对花生四烯酸血管作用以及对离体大鼠心脏中前列腺素生成量的影响。通过主动脉插管向心脏一次性注射花生四烯酸（33纳摩尔）会引起血管收缩，随后是持久的血管舒张。花生四烯酸还显著增加了心脏中前列腺素E2和6-酮-前列腺素F1α的生成量。在对乙酰氨基酚（0.1 - 1.0毫摩尔）存在的情况下，前列腺素的生成量以及冠状动脉舒张的持续时间均减弱。我们认为，花生四烯酸诱导的冠状动脉舒张的主要成分是通过前列腺素合成介导的，并且被对乙酰氨基酚所阻断。