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为探讨高温对机体的损伤机理和防治措施，对热应激过程肝线粒体、微粒体脂质过氧化、钙镁三磷酸腺苷酶（Ｃａ－Ｍｇ－ＡＴＰａｓｅ）的变化与联系进行了观察。结果显示，受热大鼠肝线粒体、微粒体丙二醛（ＭＤＡ）含量明显增多，并随受热时间延长而升高；受热（４２℃）１２０ｍｉｎ后大量的肝细胞变性、坏死，超微结构改变明显。脱离热接触６ｈ，肝线粒体ＭＤＡ含量恢复到对照组水平，但微粒体ＭＤＡ明显升高。肝线粒体ＭＤＡ含量增多，Ｃａ－Ｍｇ－ＡＴＰａｓｅ活性下降；ＭＤＡ含量降至对照组水平时，Ｃａ－Ｍｇ－ＡＴＰａｓｅ活性恢复到对照组水平。提示，经一定时间热应激后脱离热环境后，肝线粒体脂质过氧化可恢复，而微粒体脂质过氧化不易恢复；热应激肝线粒体ＭＤＡ含量与Ｃａ－Ｍｇ－ＡＴＰａｓｅ活性变化存在一定联系。
To explore the mechanism of high temperature damage to the body and its prevention and treatment measures, changes of liver mitochondria, microsomal lipid peroxidation and Ca-Mg-ATPase in the process of heat stress were observed. The results showed that the contents of malondialdehyde (MDA) in liver mitochondria and microsome of the rats increased obviously and increased with the prolongation of heating time; a large number of hepatocytes degeneration, necrosis and ultrastructure changed obviously after heated at 42 ℃ for 42 minutes . After 6h exposure to heat, the content of MDA in liver mitochondria returned to the level of control, but the content of MDA in microsome increased significantly. The content of MDA in liver mitochondria increased and the activity of Ca-Mg-ATPase decreased. When the content of MDA decreased to the level of control, the activity of Ca-Mg-ATPase returned to the control level. It is suggested that the lipid peroxidation of liver mitochondria may recover and the lipid peroxidation of microsome is not easy to recover after the thermal stress is removed from the thermal environment in a certain period of time. The changes of mitochondrial MDA content and Ca-Mg-ATPase activity There is a certain link.