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本实验在离体灌流败血症休克大鼠心脏模型上,观察到晚期败血症休克时,心肌和心肌线粒体钙含量分别增加190和332(P0.01),~LCa摄入量增加208和178。(P0.01),心肌钙释放量无明显变化 用10mol/L降钙素基因相关肽(CGRP)或10mol/L心房钠尿肽(ANP)灌流离体心脏明显减轻休克时心肌和心肌线粒体的钙超负荷,体外实验观察线粒体摄钙储备的能力,休克时心肌线粒体最大摄钙量减少31.6,摄钙速率降低33％,(P0.01)结论认为,晚期败血症休克,心肌净钙流入量显著增加和线粒体钙转运能力降低导致其对胞浆钙缓冲能力减弱是心肌细胞钙超负荷发生的重要环节CGRP,ANP可显著减轻休克时心肌和线粒体钙超负荷,在休克过程中可能对细胞有保护意义。
In this study, we found that in the rat model of isolated perfused sepsis, the mitochondrial calcium content in myocardium and myocardium increased by 190 and 332, respectively (P <0.01), and the increase of ~ LCa increased by 208 and 178, respectively. (P <0.01). There was no significant change in myocardial calcium release. Perfusion of isolated heart with 10mol / L calcitonin gene related peptide (CGRP) or 10mol / L atrial natriuretic peptide (ANP) significantly reduced myocardial and myocardial mitochondrial Calcium overload, in vitro experiments to observe the capacity of mitochondrial calcium storage, mitochondria maximum myocardial calcium intake decreased by 31.6, the rate of calcium decreased by 33%, (P <0.01) concluded that advanced sepsis shock, myocardial calcium influx significantly Increased and decreased mitochondrial calcium transport capacity leading to its weakening of cytoplasmic calcium buffer is an important part of calcium overload of cardiomyocytes CGRP, ANP can significantly reduce myocardial and mitochondrial calcium overload in shock, the process of shock may be on the cell protection significance.