氧衍生自由基在实验性休克发病机制中的作用

Oxygen-derived free radicals in the pathogenesis of experimental shock.

作者信息

Novelli G P, Angiolini P, Livi P, Paternostro E

机构信息

Institute of Anesthesiology and I.T., University of Florence, Careggi Hospital, Italy.

出版信息

Resuscitation. 1989 Dec;18(2-3):195-205. doi: 10.1016/0300-9572(89)90022-1.

DOI:10.1016/0300-9572(89)90022-1

PMID:2555873

Abstract

Oxygen-derived free radicals are naturally produced in biological systems mostly in ischemia and hypoxia related conditions. Imbalance of physiological defenses against oxygen-derived free radicals causes cellular damage. In our laboratory the role of oxygen radicals in the pathogenesis of circulatory shock was studied by exploiting the scavenging action of the spin-trapping compound phenyl-butyl-nitrone (PBN) in experiments concerning: (1) survival after shock, (2) microcirculatory derangements in endotoxin shock, (3) fluidity modifications of cell membranes during shock, (4) exhalation of ethane as non-invasive marker of shock. In some experiments the steroid methylprednisolone was used. Results showed that administration of PBN and of the steroid (1) ensures survival after otherwise lethal shock as confirmed by decreased ethane exhalation, (2) prevents microcirculatory troubles, (3) maintains stability of cell membranes. These findings strongly support the role of oxygen-derived free radicals in the pathogenesis and pathophysiology of circulatory shock.

摘要

氧衍生自由基在生物系统中主要在与缺血和缺氧相关的情况下自然产生。针对氧衍生自由基的生理防御失衡会导致细胞损伤。在我们实验室中，通过利用自旋捕获化合物苯基丁基硝酮（PBN）的清除作用，在以下实验中研究了氧自由基在循环性休克发病机制中的作用：（1）休克后的存活率，（2）内毒素休克中的微循环紊乱，（3）休克期间细胞膜流动性的改变，（4）乙烷呼出作为休克的非侵入性标志物。在一些实验中使用了类固醇甲基强的松龙。结果表明，给予PBN和类固醇：（1）如乙烷呼出减少所证实的那样，确保了在原本致命的休克后存活，（2）预防了微循环问题，（3）维持了细胞膜的稳定性。这些发现有力地支持了氧衍生自由基在循环性休克发病机制和病理生理学中的作用。