摘要
用E.Coli内毒素复制休克模型。将内毒素注入静脉后立即引起ABP先降、后升、再降的双向反应。在ABP第二次降至<8.0 kPa时,迅速采血样检查,结果为:血气无异常(P>0.05),血液pH降低(p<0.001);动脉血中葡萄糖水平降低(P<0.001),乳酸和NPN升高(P<0.01,P<0.05),胰岛素水平无明显变化(P>0.05)。预先应用654-2后再进行同样实验,发现:PaO_2-PrO_2差出现代偿性增大(p<0.05),乳酸回降至正常水平,pH显著回升(P<0.05),低血糖症明显改善(P<0.05),只是对高氮质血症无影响(P>0.05)。再将休克和654-2+休克2组的ABP作动态对比观察,未见654-2对ABP有任何影响。单纯休克的血糖水平随ABP而进行性降低;在ABP2次下降前,即注内毒素后30 min再静脉注入肾上腺素,血糖仍有升高反应,在观察期内一直在正常水平之上。作者结合实验结果对发病过程作了分析。
The shock was reproduced by injection of inactive E. Coli endotoxin intra-venous in rat. There were two phases in reaction of ABP after administration of endotoxin immediately, when the ABP fell to<8.0 kPa, second the arterial and central venous blood example were drawn to analyze, the results were as follows: the blood gases, PaO_2-PvO_2 difference and the level of insulin in plasma didn't changed significantly, the concentration of lactate and NPN in plasma increased (P<0.001), the blcod pH deereased (P<0.001). After the rat pretrcated with 654-2 the hyperiactacidemia disappeared the hypoglycemia improved significantly (P<0.05), the blood pH rose baekward near to control but still was abnormal (P<0.05), only the hyper-nitremia didn't changed. In endotoxic shock,ABP decreased progressively which was not influenced by pre-treated with 654-2, the blood sugar decreased continually, that was in keeping synchronization with ABP falling; when the rat received epinephrine iv. at 30 minute after injection of endotoxin,the plasma glucose increased instead of hypoglycemia, In this paper the pathogenesis of shock was discussed.
关键词
内毒素
休克
胰岛素
山莨菪碱
endotoxic shock
insulin
blood sugar
hyperlactacidemia
hyper-nitremia
