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血管活性介质对大鼠静脉注射花生四烯酸血压效应的相关性。

Relevance of vasoactive mediators for the blood pressure effects of intravenous arachidonic acid injection in rats.

作者信息

Heinroth-Hoffmann I, Giessler C, Mest H J

机构信息

Department of Pharmacology and Toxicology, Martin Luther University Halle-Wittenberg, Germany.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1992 Jul;46(3):197-201. doi: 10.1016/0952-3278(92)90070-y.

DOI:10.1016/0952-3278(92)90070-y
PMID:1508952
Abstract

Vasopressor response and release of eicosanoids following intravenous injection of arachidonic acid (AA) were examined in normotensive rats. AA administration caused a rapid initial fall of arterial pressure followed by a brief rise and a subsequent prolonged fall in anesthetized rats. Immediately after AA injection the blood levels of TXB2 and 6-keto-PGF1 alpha, the stable metabolites of TXA2 and prostacyclin, rose, from 1.52 +/- 0.23 ng/ml to 176.4 +/- 42.6 ng/ml and from 4.05 +/- 0.67 ng/ml to 171.4 +/- 31.2 ng/ml, respectively. Blood pressure behaviour and eicosanoid blood level were influenced by different inhibitors and antagonists of vasoactive mediators. The cyclooxygenase inhibitor acetylsalicylic acid completely eliminated the second blood pressure depression after AA injection and simultaneously diminished TXB2 and 6-keto-PGF1 alpha formation in murine blood, whereas the TXA2 receptor antagonist BM 13.177 prevented the return of the blood pressure to preinjection level after the initial brief fall in arterial pressure. Although the TXA2 synthase inhibitor HOE 944 markedly inhibited TXB2 formation, no influence on AA-induced blood pressure changes could be registered. The receptor antagonist of platelet activating factor BN 52021 and the serotonin and histamine receptor antagonist cyproheptadine also reduced TXB2 amounts, in murine blood without any effects on blood pressure behaviour.

摘要

在正常血压大鼠中,研究了静脉注射花生四烯酸(AA)后血管加压反应和类花生酸的释放。给麻醉大鼠注射AA后,动脉压先迅速下降,随后短暂上升,接着持续下降。注射AA后立即检测,血栓素A2(TXA2)和前列环素的稳定代谢产物TXB2和6 - 酮 - PGF1α的血药浓度分别从1.52±0.23 ng/ml升至176.4±42.6 ng/ml以及从4.05±0.67 ng/ml升至171.4±31.2 ng/ml。血管活性介质的不同抑制剂和拮抗剂会影响血压变化行为和类花生酸血药浓度。环氧化酶抑制剂乙酰水杨酸完全消除了注射AA后的第二次血压下降,并同时减少了小鼠血液中TXB2和6 - 酮 - PGF1α的生成,而TXA2受体拮抗剂BM 13.177在动脉压最初短暂下降后可防止血压恢复到注射前水平。尽管TXA2合酶抑制剂HOE 944显著抑制TXB2的生成,但未观察到其对AA诱导的血压变化有影响。血小板活化因子受体拮抗剂BN 52021以及5 - 羟色胺和组胺受体拮抗剂赛庚啶也可降低小鼠血液中TXB2的含量,但对血压变化行为无任何影响。

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