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目的：探讨脑卒中后血糖升高的机制。方法：采用葡萄糖氧化酶－过氧化酶法和同位素放射免疫法对脑卒中急性期血糖和促肾上腺皮质激素、皮质醇、胰高血糖素、生长素、胰岛素、甲状腺素及三碘甲状腺原氨酸浓度进行动态测定，对血糖和上述激素浓度变化与脑中线移位、脑室受压、血肿破入脑室进行相关性研究。结果：脑卒中后血糖浓度与出血、梗死体积正相关。病变部位在基底节区者高血糖的发生率明显升高。高血糖组血糖升高时促肾上腺皮质激素浓度明显高于血糖降至正常后、脑卒中后正常血糖组和对照组。高血糖、促肾上腺皮质激素浓度升高与脑中线移位、脑室受压、血肿破入脑室有关。血糖浓度与皮质醇、胰高血糖素浓度呈正相关，与Ｔ３负相关。结论：脑出血、脑梗死后血糖升高的机制可能与脑中线移位、脑室受压、血肿破入脑室等刺激下丘脑，引起促肾上腺皮质激素、胰高血糖素释放因子释放增加，继而血中皮质醇、胰高血糖素浓度升高、三碘甲状腺原氨酸浓度降低有关。
Objective: To explore the mechanism of blood sugar after stroke. Methods: Glucose oxidase-peroxidase and radioimmunoassay were used to detect the levels of blood glucose and adrenocorticotropic hormone, cortisol, glucagon, auxin, insulin, thyroxine and triiodothyronine Concentration dynamic determination of blood glucose and the above hormone concentration and brain midline displacement, ventricular compression, hematoma rupture of the ventricular correlation study. Results: The blood glucose level after stroke was positively correlated with the volume of hemorrhage and infarction. Lesions in patients with basal ganglia were significantly higher incidence of hyperglycemia. Hyperglycemia group elevated serum adrenocorticotropic hormone concentration was significantly lower than normal after blood glucose, stroke and normal blood glucose control group. Hyperglycemia, adrenocorticotropic hormone concentrations and brain midline shift, ventricular compression, hematoma ruptured into the ventricle. Blood glucose concentration and cortisol, glucagon concentration was positively correlated with T3 negative correlation. Conclusion: The mechanism of elevated blood glucose after cerebral hemorrhage and cerebral infarction may be related to the midline shift, ventricular compression, hematoma rupture into the ventricles and other stimuli hypothalamus, causing adrenocorticotropic hormone, glucagon release factor release increased, followed by blood Cortisol, glucagon concentration, triiodothyronine concentration decreased.