论文部分内容阅读
在离休大鼠心脏缺血再灌损伤模型上，研究水杨酸钠（ＳＡ）对缺血再灌后心功能恢复及心肌组织Ｃａ２＋含量的影响。与缺血再灌组比较，ＳＡ（０．１－１．０ｍｍｏｌ·Ｌ－１）呈剂量依赖性显著抑制心脏再灌后心功能的恢复。心肌组织Ｃａ２＋含量显著增高。络合剂ＥＤＴＡ和小牛血清白蛋白均能显著对抗ＳＡ诱导的心功能损害，使心肌组织Ｃａ２＋含量显著降低。提示ＳＡ能加重离休大鼠心脏缺血再灌损伤。其机理可能与其促进Ｃａ２＋超负荷引起的心肌损伤有关。ＥＤＴＡ和小牛血清白蛋白具有对抗ＳＡ的心肌毒性作用。
To investigate the effect of sodium salicylate (SA) on the recovery of cardiac function and the content of Ca2 + in myocardium after ischemia / reperfusion injury in reperfusion injury model in rats. Compared with ischemia reperfusion group, SA (0.1-1.0mmol·L-1) significantly inhibited the recovery of cardiac function after cardiac reperfusion in a dose-dependent manner. Myocardial Ca2 + content was significantly higher. Complexing agent EDTA and bovine serum albumin can significantly antagonize SA-induced cardiac dysfunction, myocardial Ca2 + content was significantly reduced. It suggested that SA could aggravate the ischemic and reperfusion injury of retired rats. The mechanism may be related to its promotion of myocardial injury caused by Ca2 overload. EDTA and bovine serum albumin have a cardiotoxic effect against SA.