钠氢交换体的活性会导致缺血再灌注后的心脏损伤。

Activity of the Na+/H+ exchanger contributes to cardiac damage following ischaemia and reperfusion.

Allen D G, Xiao X H

Institute for Biomedical Research, Department of Physiology, University, of Sydney, New South Wales, Australia.

Clin Exp Pharmacol Physiol. 2000 Sep;27(9):727-33. doi: 10.1046/j.1440-1681.2000.03329.x.

Abstract

The present review considers the evidence that Na+-H+ exchange activity contributes to cardiac damage following ischaemia and reperfusion. The basic mechanism involved is that protons are produced during ischaemia and leave the myocytes on the Na+/H+ exchanger during either ischaemia and/or reperfusion. The resulting elevation of [Na+]i causes Ca2+ loading through the Na+/Ca2+ exchanger and the elevated [Ca2+]i is thought to lead to myocardial damage. 2. Inhibition of the Na+/H+ exchanger during ischaemia and/or reperfusion produces a substantial cardioprotective effect by blocking the damage caused by the coupled exchanger mechanism described above. Preconditioning also produces a cardioprotective effect and the evidence that this also involves the Na+/H+ exchanger is reviewed. 3. The intracellular mechanisms associated with ischaemic damage and preconditioning are of great interest because they may provide targets for potential therapeutic interventions. The intracellular regulation of the Na+/H+ exchanger appears to be an important component of these pathways and may become a focus for therapeutic approaches.

摘要

本综述探讨了钠氢交换活性导致缺血再灌注后心脏损伤的证据。其涉及的基本机制是，缺血期间会产生质子，在缺血和/或再灌注期间，质子通过钠氢交换体离开心肌细胞。由此导致的细胞内钠离子浓度升高会通过钠钙交换体使钙离子内流增加，而升高的细胞内钙离子浓度被认为会导致心肌损伤。2. 在缺血和/或再灌注期间抑制钠氢交换体，可通过阻断上述耦合交换体机制所造成的损伤，产生显著的心脏保护作用。预处理也可产生心脏保护作用，本文将对其也涉及钠氢交换体的证据进行综述。3. 与缺血损伤和预处理相关的细胞内机制备受关注，因为它们可能为潜在的治疗干预提供靶点。钠氢交换体的细胞内调节似乎是这些途径的重要组成部分，可能成为治疗方法的重点。