Kazueva T V, Kvasha L V, Seleznev S A
Biull Eksp Biol Med. 1984 Jun;97(6):666-7.
In contrast to the reported data evidencing early impairment of the liver mitochondrial function in the Wiggers model of hemorrhagic shock at the arterial blood pressure 30-40 mm Hg, lasting not over 6 h, a group of hemorrhage-resistant rats was discovered. In these rats, the lifetime was about 20 h, with the blood pressure being the same as indicated above. Rectal temperature decreased to 24-25 degrees C during shock. No substantial disorders were recorded in oxidative phosphorylation and ATPase activity of the mitochondria isolated from the liver in the irreversible stage of shock (70% blood return) or in the terminal state of animals. It is assumed that hypothermia plays the protective role. The conclusion is made that the damage to the mitochondria is not indispensable factor of the development of irreversible shock.
与报道的数据相反，在动脉血压为30 - 40 mmHg、持续不超过6小时的维格斯失血性休克模型中，肝脏线粒体功能早期受损，而我们发现了一组抗出血大鼠。这些大鼠的存活时间约为20小时，血压与上述相同。休克期间直肠温度降至24 - 25摄氏度。在休克不可逆阶段（回输70%血液）或动物终末期，从肝脏分离的线粒体的氧化磷酸化和ATP酶活性未记录到明显紊乱。推测体温过低起到了保护作用。得出的结论是，线粒体损伤不是不可逆休克发展的必要因素。
