论文部分内容阅读
目的研究大鼠心室肌细胞在代谢性抑制预处理中钠/钙交换体(NCX)反向转运的活性,以及NCX反向转运抑制剂是否可以阻止代谢性抑制预处理后的心肌保护作用。方法酶解法分离制备钙耐受心肌细胞,用Fura2/AM负载,采用双激发荧光光电倍增系统(IonOptixPhotometrySystem)检测钙信号,用单心肌细胞动缘探测技术观察心肌细胞收缩/舒张功能,台盼蓝染色法检测细胞存活率。结果在代谢性抑制预处理30min时,NCX反向转运被激活。NCX反向转运抑制剂KBR7943(0.5μmol/L)可以抑制代谢性抑制预处理对心肌细胞收缩功能和细胞存活率的作用。NCX激动剂E4031(1μmol/L)可以模拟代谢性抑制预处理后对心肌细胞收缩功能的保护作用,这一作用也可被KBR7943阻断。结论代谢性抑制预处理中,NCX反向转运的激活触发了代谢性抑制预处理后的心肌保护作用;NCX的抑制剂可以阻止代谢性抑制预处理后的心肌保护作用。
Objective To investigate the antiporter activity of sodium / calcium exchanger (NCX) in rat ventricular myocytes during metabolic inhibition and whether NCX reverse transport inhibitors can prevent myocardial protection after metabolic inhibition of preconditioning. Methods Calcium-resistant cardiomyocytes were isolated by enzymatic hydrolysis and loaded with Fura2 / AM. Calcium signals were detected by dual-excitation fluorescence photomultiplication system (IonOptixPhotometrySystem). Cardiomyocyte contractile / diastolic function was observed by single cardiomyocyte electrophysiological detection. Trypan blue Cell viability was detected by staining. Results NCX reverse transport was activated at 30min after metabolic inhibition. NCX reverse transport inhibitor KBR7943 (0.5μmol / L) can inhibit the metabolic inhibition of preconditioning on myocardial cell contractile function and cell survival rate. The NCX agonist E4031 (1μmol / L) can mimic the protective effect of metabolic inhibition on contractile function of cardiomyocytes after pretreatment, and this effect can be blocked by KBR7943. Conclusions Activation of NCX reverse transport triggers cardioprotection after metabolic inhibition pretreatment in metabolic inhibition pretreatment. Inhibitors of NCX can prevent myocardial protection after metabolic inhibition of preconditioning.