Lee Candace, Dhalla Naranjan S, Hryshko Larry V
Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Can J Cardiol. 2005 May 1;21(6):509-16.
The cardiac Na+-Ca2+ exchanger (NCX) plays an essential role in regulating Ca2+ under physiological and pathophysiological conditions. In its forward mode of operation, which predominates under physiological conditions, it extrudes the Ca2+ that enters the cardiac myocyte on a beat-to-beat basis. During ischemia and reperfusion, increased intracellular Na+ leads to a decrease in Ca2+ efflux and enhanced Ca2+ influx via the NCX, potentially leading to Ca2+ overload, which is one of the major pathophysiological mechanisms for ischemia-reperfusion injury. Novel NCX inhibitors discovered in recent years have shown great promise in attenuating ischemia-reperfusion injury.
心脏钠钙交换体（NCX）在生理和病理生理条件下对钙的调节起着至关重要的作用。在其正向运转模式下（在生理条件下占主导），它逐搏排出进入心肌细胞的钙。在缺血和再灌注期间，细胞内钠增加导致钙外流减少，并通过NCX增强钙内流，这可能导致钙超载，而钙超载是缺血再灌注损伤的主要病理生理机制之一。近年来发现的新型NCX抑制剂在减轻缺血再灌注损伤方面显示出巨大潜力。
