心肌缺血—再灌注损伤与心肌去甲肾上腺素的释放

The release of endogenous norepinephrine in the postischemic reperfused myocardium in the rabbits

家兔急性开胸实验,结扎冠状动脉左室支35分钟后,去除结扎(再灌注)10分钟,发现心脏功能较单纯结扎组明显降低,再灌注区心肌去甲肾上腺素(NA)含量显著降低,同时伴有组织Ca^(++)含量显著升高。测定血钙和组织含水量结果提示,再灌注后心肌Ca^(++)含量的升高系由Ca^(++)在细胞内的堆积所致。再灌注损伤可能与再灌注过程中心肌组织内源性儿茶酚胺大量释放有关。

Various studies have suggested that adrcnergic activtaion may contribute to deleterious effects on myocardial ischemia. However, very little is known about it s role during reperfusion. This study was designed to explore the relationship between endogenous norepinephrine (NE) and reperfusion injury in intact rabbits. In rabbits(n=5) 35 min of coronary occlusion without reperfusion thc myocardial NE content of the ischemic area was not significantly different from that of the non-ischemic area, nor was tissue calcium content in both areas, while, in 35 min of occlusion followed by 10 min of reperfusion group(n=5), the tissue NE was markedly reduced in reperfused area accompanying significant calcium overloading. These studies suggest that the postischemic reperfusion injury may be, in part, due to endogenous catecholamine release during reperfusion.