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酸性pH对灌注大鼠肝脏缺氧性细胞杀伤的保护作用:pH值矛盾的证据。

Protection by acidotic pH against anoxic cell killing in perfused rat liver: evidence for a pH paradox.

作者信息

Currin R T, Gores G J, Thurman R G, Lemasters J J

机构信息

Department of Cell Biology and Anatomy, University of North Carolina, Chapel Hill 27599.

出版信息

FASEB J. 1991 Feb;5(2):207-10. doi: 10.1096/fasebj.5.2.2004664.

Abstract

Reperfusion of ischemic tissues causes a paradoxical injury. Here, we measured lactate dehydrogenase (LDH) release as an indicator of tissue damage in perfused rat livers during anoxia and reoxygenation. During anoxia, LDH release was substantially reduced at acidotic pH (pH 6.1-6.9). Using anoxia at pH 6.1 followed by reoxygenation at pH 7.3 to model ischemia and reperfusion, an abrupt release of LDH occurred after reperfusion. A similar release of LDH occurred when pH of anoxic livers was increased to 7.3 without reoxygenation but LDH release did not occur after reoxygenation at pH 6.1. Thus, a rapid increase of pH rather than reoxygenation accounted for tissue injury after reperfusion of ischemic liver.

摘要

缺血组织的再灌注会导致矛盾性损伤。在此,我们测量了乳酸脱氢酶(LDH)的释放,以此作为灌注大鼠肝脏在缺氧和复氧过程中组织损伤的指标。在缺氧期间,在酸性pH值(pH 6.1 - 6.9)下LDH释放显著减少。使用pH 6.1的缺氧随后pH 7.3的复氧来模拟缺血和再灌注,再灌注后出现了LDH的突然释放。当缺氧肝脏的pH值在未复氧的情况下升至7.3时,也出现了类似的LDH释放,但在pH 6.1复氧后未出现LDH释放。因此,pH值的快速升高而非复氧是缺血肝脏再灌注后组织损伤的原因。

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