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目的研究脑卒中血糖升高机制。方法采用葡萄糖氧化酶法测定血糖和微栓柱法测定GhbA1c,采用放射免疫法测定血皮质醇(COR)、胰岛素(INS)、胰高血糖素(GCG)及促肾上腺皮质激素(ACTH)。卒中组与对照组均数比较采用t检验作对比分析。结果脑卒后高血糖组血ACTH,COR和GCG及INS升高;病灶位于基底节者高血糖及ACTH升高比例均高于非基底节者。结论脑卒中后血糖升高与交感-肾上腺和垂体-肾上腺系统活化及继发血中ACTH,COR和GCG等激素水平升高有关,也与病灶位于基底节区有关。对卒中后血糖升高患者应及时应用胰岛素控制应激性高血糖状态,对颅内高压脑水肿者给予脱水剂减轻对下丘脑的影响,避免进一步加重高血糖和脑损害。
Objective To study the mechanism of blood glucose in stroke. Methods GhbA1c was determined by glucose oxidase method and micro-plug method. Radioimmunoassay was used to detect COR, INS, GCG and ACTH. Stroke group and control group were compared using t test for comparative analysis. Results Serum ACTH, COR, GCG and INS were increased in patients with hyperglycemia after stroke. The percentage of elevated hyperglycemia and ACTH in the basal ganglia were higher than those in non-basal ganglia. Conclusions After stroke, the hyperglycemia is related to the activation of the sympathetic-adrenal and pituitary-adrenal system and the elevation of the levels of ACTH, COR and GCG and other hormones in the secondary blood. It is also related to the localization of the lesions in the basal ganglia. Patients with elevated blood glucose after stroke should promptly insulin-controlled stress hyperglycemia, hydrocephalus intracranial hypertension were given dehydration agent to reduce the hypothalamus, to avoid further aggravating hyperglycemia and brain damage.