内源性前列环素在心肌缺血时可维持心肌功能并促进内皮源性一氧化氮的生成。

Endogenous prostacyclin preserves myocardial function and endothelium-derived nitric oxide formation in myocardial ischemia.

作者信息

Schrör K, Woditsch I

机构信息

Institut für Pharmacokologie, Heinrich-Heine-Universität Düsseldorf, FRG.

出版信息

Agents Actions Suppl. 1992;37:312-9. doi: 10.1007/978-3-0348-7262-1_43.

DOI:10.1007/978-3-0348-7262-1_43

PMID:1632306

Abstract

Nitric oxide (NO) and prostacyclin (PGI2) release was determined in effluents of Langendorff-perfused rabbit hearts under control conditions and during reperfusion subsequent to 2 h of global, low-flow ischemia. PGI2 release (6-oxo-PGF1 alpha) was significantly enhanced during early reperfusion and remained enhanced during a total time of 70 min of reperfusion. NO formation was reduced during ischemia but was substantially enhanced during reperfusion. Inhibition of endogenous PGI2 production by indomethacin resulted in severe disturbance of myocardial function and NO release. Inhibition of NO generation by L-N-nitroarginine did not affect myocardial contractility. These data suggest a cardioprotective and endothelium-protective role of PGI2 in myocardial ischemia which also involves protection of NO generation.

摘要

在对照条件下以及在2小时全心低流量缺血后的再灌注期间，测定了Langendorff灌注兔心脏流出液中一氧化氮（NO）和前列环素（PGI2）的释放。PGI2释放（6-氧代-PGF1α）在再灌注早期显著增强，并在总共70分钟的再灌注期间持续增强。NO生成在缺血期间减少，但在再灌注期间大幅增强。吲哚美辛抑制内源性PGI2生成导致心肌功能和NO释放严重紊乱。L-N-硝基精氨酸抑制NO生成并不影响心肌收缩力。这些数据表明PGI2在心肌缺血中具有心脏保护和内皮保护作用，这也涉及对NO生成的保护。