摘要
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。
In the blood plasma, the levels of insulin, gluco-corticoid, glucose, lactate and non-protein-ni-trogen rose and free fatty acid fell 2 hours after hemorrhagic shock, which were the typical features of tissue insulin resistance. When the animal pre-treated with 654-2, the hyper—glycemia recovered partially, the other metabolic changes returned to control; but the two kinds of hormones reacting to shock did not be influenced. The above experimental results showed that the mechanism initiating the abnormal metabolic response to hemorrhagic shock was that the tissue was significantly depressed insensitivity to the effect of insulin. Anisodamine ensured the tissue aganist the impairment of shock,the normal ability of tissue to react to the stimulation of insulin was preserved, so the tissue would uti-lize oxygen by aid of compensatorystore of oxygen dissociation continuously in the low blood flow per-fusion. Under such condition, the disturbances of metabolism were abolished, the tissue insulin resis-tance was prevented. According to a series of previous studies in our laboratory and the information of other scholars, we considered that the endotoxin invading from intestine was assumed to be the prima-ry factor impairing cell to occur insulin resistance, and not that cell had no oxygen to utilized but that it had impaired ability to use it.
基金
国家自然科学基金
关键词
失血性
休克
胰岛素拮抗
物质代谢
hemorrhagic shock
insulin resistance:material metabolism
