格列本脲可防止异氟烷对缺血后再灌注大鼠心脏中羟自由基形成的降低作用。

Glyburide prevents isoflurane's reducing effects on hydroxyl radical formation in the postischemic reperfused rat heart.

作者信息

Yamaguchi Toshiaki, Kashimoto Satoshi, Oguchi Takeshi, Kumazawa Teruo

机构信息

Department of Anesthesiology, Yamanashi Medical University, Yamanashi, Japan.

出版信息

Exp Clin Cardiol. 2002 Spring;7(1):25-9.

PMID:19644575

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2716186/

Abstract

BACKGROUND

The role of K(ATP) channels in isoflurane's reducing effects on oxygen free radical formation are not well known.

OBJECTIVES

To investigate whether glyburide, an ATP-regulated potassium (K(ATP)) channel blocker, abolishes isoflurane-induced cardioprotective effects and whether it affects hydroxyl radical formation in the postischemic reperfused heart.

ANIMALS AND METHODS

Thirty-nine male Wistar rats were divided into four groups: group C (control, n=10), group I (isoflurane, n=9), group G (glyburide, n=10) and group GI (glyburide and isoflurane, n=10). The hearts were perfused as a Neely's working heart model. Afterwards, global heart ischemia was induced for 15 min followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent and heart was measured with high performance liquid chromatography.

RESULTS

Isoflurane alone and glyburide alone produced significant decreases in the duration of ventricular fibrillation during reperfusion (group C 452+/-345, group I 247+/-60, group G 261+/-135 s; P<0.05). In the presence of glyburide, isoflurane did not further decrease the duration of arrhythmia (group GI 230+/-48 s). Isoflurane reduced hydroxyl radical formation significantly in the coronary effluent during ischemia and reperfusion, but this was prevented by glyburide.

CONCLUSION

The results suggest that isoflurane reduces hydroxyl radical formation, at least in part, through activation of K(ATP) channels.

摘要

背景

ATP敏感性钾（K(ATP)）通道在异氟烷降低氧自由基形成方面的作用尚不清楚。

目的

研究ATP调节的钾（K(ATP)）通道阻滞剂格列本脲是否能消除异氟烷诱导的心脏保护作用，以及它是否影响缺血再灌注心脏中羟自由基的形成。

动物与方法

39只雄性Wistar大鼠分为四组：C组（对照组，n = 10）、I组（异氟烷组，n = 9）、G组（格列本脲组，n = 10）和GI组（格列本脲与异氟烷组，n = 10）。心脏作为Neely工作心脏模型进行灌注。之后，诱导全心缺血15分钟，随后再灌注20分钟。用高效液相色谱法测定冠状动脉流出液和心脏中羟自由基的形成。

结果

单独使用异氟烷和单独使用格列本脲均可使再灌注期间室颤持续时间显著缩短（C组452±345、I组247±60、G组261±135秒；P<0.05）。在格列本脲存在的情况下，异氟烷并未进一步缩短心律失常的持续时间（GI组230±48秒）。异氟烷可显著减少缺血和再灌注期间冠状动脉流出液中羟自由基的形成，但这一作用被格列本脲阻断。