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失血休克2h,血中胰岛素、葡萄糖、乳酸和NPN升高,自由脂酸降低,这是典型的胰岛素拮抗现象。此外,血中糖皮质激素也显著升高。预先应用654-2后,虽未扩容救治、但升高的血糖回降一半左右,其余的代谢变化则完全消失;654-2对升高的胰岛素和糖皮质激素却无明显影响,只改变代谢变化而不影响调节激素的反应,说明胰岛素拮抗的发生是休克损伤了细胞所致。654-2可保护细胞的结构与功能使其对胰岛素反应正常,并继续动用远未耗竭的血氧解离代偿的储备,从而使各项代谢障碍消除或改善。以上结果表明,作者曾提出的失血休克的细胞并非无氧可用而是用氧障碍之说是可以成立的。我们根据以往的工作和文献复习,认为失血休克过程损伤细胞使其对胰岛素反应性降低的因素可能主要是肠源性内毒素。
2h after hemorrhagic shock, the blood insulin, glucose, lactate and NPN increased free fatty acid decreased, which is a typical phenomenon of insulin antagonism. In addition, blood glucocorticoid is also significantly increased. Pre-application of 654-2, although not expansion of the treatment, but elevated blood sugar about half fallback, the remaining metabolic changes completely disappeared; 654-2 on insulin and glucocorticoid increased but no change, only changes in metabolism Changes do not affect the response to regulate hormones, indicating that the occurrence of insulin resistance is shock caused by damage to the cells. 654-2 protects the cell’s structure and function, making it responsive to insulin and continuing to use far-depleted oxygen dissociation compensated reserves to eliminate or improve various metabolic disorders. The above results show that the authors have proposed that the cells of the hemorrhagic shock can not be established without oxygenation but with oxygen disorder. Based on our previous work and review of the literature, we concluded that the factor that impairs the ability of cells to respond to insulin in the course of hemorrhagic shock may be mainly enterotoxin.