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本文观察了早期，晚期败血症休克大鼠肝脏内质网钙ＡＴＰ酶磷酸化的改变。败血症休克模型由结扎大鼠盲肠并穿孔（ＣＬＰ）的方法复制。采用蔗糖密度梯度离心法分离肝脏内质网。由聚丙烯酰胺凝胶电泳（ＳＤＳ－ＰＡＧＥ）鉴定肝脏内质网钙ＡＴＰ酶磷酸化中间产物。结果发现，肝脏粗面内质网，中间内质网，滑面内质网钙ＡＴＰ酶磷酸化能力在败血症休克早期降低１５－２３％，晚期降低１７－２７％（ｐＭＯ．０５）。动力学分析发现，早期、晚期败血症休克时，钙离子、ＡＴＰ对钙ＡＴＰ酶磷酸化的最大反应速度都明显降低，而Ｋｍ值无明显变化。ＳＤＳ－ＰＡＧＥ分析证实，肝脏内质网钙ＡＴＰ酶磷酸化的中间产物是一个分子量为１１５ｋＤ的蛋白质。结论认为：败血症休克时，肝脏内质网钙ＡＴＰ酶磷酸化能力明显减低，去磷酸化能力无明显变化，可能是败血症休克时肝细胞钙稳态失衡进而引起机体代谢改变的主要原因之一。
This article observed early and advanced sepsis hepatic endoplasmic reticulum calcium ATPase phosphorylation changes. Septic shock model was replicated by ligation of rat cecal and perforation (CLP). Liver endoplasmic reticulum was separated by sucrose density gradient centrifugation. Liver endoplasmic reticulum calcium ATPase phosphorylation intermediate was identified by polyacrylamide gel electrophoresis (SDS-PAGE). The results showed that the hepatic rough endoplasmic reticulum, middle endoplasmic reticulum, endoplasmic reticulum calcium ATPase phosphorylation capacity in the early sepsis shock reduced by 15-23%, late reduced by 17-27% (pMO.05). Kinetic analysis found that, in early and advanced sepsis shock, the maximal reaction rate of calcium ion and ATP on calcium ATPase phosphorylation was significantly reduced, while the Km value did not change significantly. SDS-PAGE analysis confirmed that liver endoplasmic reticulum calcium ATPase phosphorylation intermediate is a protein molecular weight of 115kD. The conclusion is that septic shock, liver endoplasmic reticulum calcium ATPase phosphorylation decreased significantly, dephosphorylation no significant change may be septic shock hepatocyte calcium homeostasis and then cause one of the main metabolic changes in the body.