Farnebo L O, Fredholm B B, Hamberger B, Hjemdahl P, Westman L
Acta Chir Scand. 1977;143(1):9-14.
Hemorrhagic shock was induced in rats by bleeding to 35 mmHg for a period of 4 h. Plasma glucose increased rapidly following the onset of bleeding and reached twice the control value after 30 min. After 2 h hypotension the liver content of glycogen was depleted and subsequently the rats became hypoglycemic. The rise in plasma glucose was accompanied by a rise in plasma cyclic AMP, which was 10-fold after 1 h, but returned towards control values at the end of the hypotensive period. There were no corresponding changes in the cyclic AMP contents of liver, heart or adipose tissue. Blood lactate was increased 10-fold and the lactate/pyruvate ratio was more than doubled, suggesting an increased anaerobic metabolism. Plasma FFA levels fell significantly, while plasma glycerol was unchanged during the hypotensive period. In this hemorrhagic shock model there is an initial phase of glucose mobilization from the liver, which is accompanied by elevated plasma cyclic AMP. This phase is followed by a period of depressed levels of glucose as well as FFA and thus a lack of metabolizable substrates in plasma.
通过将大鼠血压降至35 mmHg并持续4小时来诱导失血性休克。出血开始后血浆葡萄糖迅速升高,30分钟后达到对照值的两倍。低血压2小时后,肝脏糖原含量耗尽,随后大鼠出现低血糖。血浆葡萄糖的升高伴随着血浆环磷酸腺苷(cAMP)的升高,1小时后升高了10倍,但在低血压期结束时恢复到对照值。肝脏、心脏或脂肪组织的cAMP含量没有相应变化。血乳酸增加了10倍,乳酸/丙酮酸比值增加了一倍多,表明无氧代谢增加。血浆游离脂肪酸(FFA)水平显著下降,而低血压期间血浆甘油水平不变。在这个失血性休克模型中,最初存在肝脏葡萄糖动员阶段,同时伴有血浆cAMP升高。这个阶段之后是葡萄糖以及FFA水平降低的时期,因此血浆中缺乏可代谢底物。