【摘要】 目的　了解缺氧状态新生儿胰岛素受体水平的血糖调节机制。方法　对7 头新生小牛(缺氧组) 头罩吸入0-048 ～0-059 氧气2 小时,对照组(7 头) 吸入氧气浓度为0-208,测定乳酸及血气,观察血糖和肝组织胰岛素受体的酪氨酸蛋白激酶(TPK) 活性。结果　缺氧组呈乳酸酸中毒,血糖明显高于对照组[(8-0 ±1-3) mmol/L与(4-8±1-3) mmol/L相比,P< 0-01] ,随胰岛素刺激浓度的增加,激酶活性增高,缺氧组与对照组相比,差异有非常显著意义。结论　缺氧可诱导新生小牛血糖升高,缺氧时胰岛素受体TPK活性下降是血糖升高的原因之一更多还原

【Abstract】 Objective To understand the mechanism of regulating blood glucose in hepatic post insulin receptor level in hypoxic newborns Methods Seven newborn calves were given 4 8% 5 9% of oxygen inhalation with hoods for two hours. The control calves were given 20 8% of oxygen inhalation The lactate, blood gases, blood glucose and tyrosine specific protein kinase (TPK) activities of hepatic insulin receptors were measured Results Severe lactate acidosis existed in hypoxic group The blood glucose was much higher in hypoxic group than those in control group [(8 0±1 3) mmol/L vs (4 8±1 3) mmol/L, P< 0 01], and the TPK activities of hepatic insulin receptors were significantly lower in hypoxic group than that in control group (K0 P = 0 001, K1 P< 0 01, K2 P=0 001, K3 P< 0 01, K4 P< 0 01, K5 P< 0 01) Conclusion Hypoxia could induce an increase of blood glucose in newborn calves and one of the mechanisms for regulation of blood glucose might be the decrease of tyrosine protein activeities of the insulin receptor更多还原