Mizobe T, Okuda C
Department of Anesthesiology, Kyoto Prefectural University of Medicine, Japan.
Circ Shock. 1988 Nov;26(3):245-56.
Alterations in thyrotropin-releasing hormone (TRH) content in the brain during hemorrhagic shock were examined in conscious rats, and the results were interpreted in relation to the reversibility of the shock. Two sets of experiments were run. The first one was to establish reversible and irreversible shock models. Hemorrhagic shock was induced by the initial withdrawal of 4 ml of blood followed by 1 ml bleeds at 5, 15, 30, and 60 min to maintain the blood pressure at 40-70 mmHg for 60 min. Blood withdrawn during and 60 min after the end of the shock was used to measure plasma lactate levels and blood gases. Shock was considered to be reversible if the animal survived for 24 hr after the hemorrhage. The plasma lactate levels as well as Base Excess and PaCO2 during and 60 min after the end of the hemorrhage of the surviving rats were significantly different from those of the animals which died within 24 hr. In particular, the plasma lactate levels at 60 min after the end of the hemorrhagic period were good indicators of the mortality of animals; it was predicted that rats whose plasma lactate levels are higher than 3.8 mEq/L would die within 24 hr (0.69% probability of misdiscrimination). The second experiment was to measure brain TRH content during and after hemorrhage produced using the same bleeding procedure as the first. During hemorrhage, brain TRH contents in the medulla oblongata and midbrain were found to be significantly increased compared with the control values. At 60 min after the end of hemorrhage, significantly higher TRH content values were obtained in the medulla oblongata, midbrain, cerebral cortex, striatum, and cerebellum in the rats whose plasma lactate levels were lower than 3.8 mEq/L compared with those of animals having plasma lactate values higher than 3.8 mEq/L. From the results of the two sets of experiments, it is concluded that the surviving animals have more TRH in the brain regions mentioned above than the non-surviving animals after hemorrhagic shock, and it is suggested that brain TRH plays a beneficial role in the course of recovery from hemorrhagic shock.
在清醒大鼠中检测了失血性休克期间大脑中促甲状腺激素释放激素(TRH)含量的变化,并结合休克的可逆性对结果进行了解释。进行了两组实验。第一个实验是建立可逆性和不可逆性休克模型。通过最初抽取4毫升血液,然后在5、15、30和60分钟时每次抽取1毫升血液来诱导失血性休克,使血压维持在40 - 70毫米汞柱60分钟。在休克期间及休克结束后60分钟抽取的血液用于测量血浆乳酸水平和血气。如果动物在出血后存活24小时,则认为休克是可逆的。存活大鼠在出血期间及出血结束后60分钟的血浆乳酸水平以及碱剩余和动脉血二氧化碳分压与在24小时内死亡的动物有显著差异。特别是,出血期结束后60分钟的血浆乳酸水平是动物死亡率的良好指标;预测血浆乳酸水平高于3.8毫当量/升的大鼠将在24小时内死亡(误判概率为0.69%)。第二个实验是使用与第一个相同的放血程序,测量出血期间及出血后的大脑TRH含量。在出血期间,与对照值相比,延髓和中脑中的大脑TRH含量显著增加。在出血结束后60分钟,血浆乳酸水平低于3.8毫当量/升的大鼠的延髓、中脑、大脑皮层、纹状体和小脑中的TRH含量值显著高于血浆乳酸值高于3.8毫当量/升的动物。从两组实验的结果得出结论,失血性休克后,存活动物在上述脑区中的TRH比未存活动物更多,并且表明大脑TRH在失血性休克的恢复过程中发挥有益作用。