高血糖、胰岛素抵抗与脑缺血性损伤

目的:探讨急性脑梗死后高血糖与胰岛素抵抗的作用及相互关系。方法:选取我院非腔隙性脑梗死住院病人50例作为实验组,依据血糖水平将其分为A组22例(单纯性高血糖)及B组(血糖正常)28例。分别在起病24h内、48h、72h、5d及9d测定患者血清中的神经元特异性烯醇酶(NSE)作为脑缺血损伤的生化标志;同时在急性期和恢复期测定空腹血糖(FPG)及空腹胰岛素(FINS),分别计算胰岛素敏感指数(ISI)及NSE释放曲线下面积。结果:实验组NSE呈动态升高,ISI值明显降低,而A组ISI值降低更明显;A组与B组相比,NSE高峰后移及峰值加大;NSE曲线下面积主要与升高的血糖有关,而与血中胰岛素水平及ISI相关性不显著。结论:高血糖加重脑缺血性损伤:胰岛素抵抗是脑梗死的危险因素,但对脑损伤的作用不明显。

Role of Hyperglycemia and Insulin Resistance in Acute Cerebral Ischemic Lesion

Objective: This study aimed to investigate the effect of compensatory hyperglycemia and insulin resistance on cerebral ischemic lesion and the relationship between them. Methods: Fifty consecutive patients with nonlacunar infarction, who were normotensive, nondiabetic, nonobese and without coronary heart disease, were classified into two groups- compensatory hyperglycemia and normoglycemia-based on the level of the fasting plasma glucose. Venous blood samples were taken after admission and at days 2,3 ,5 ,9and neuron-specific enolase (NSE) were analyzed by the use of ELISA as the marker of brain damage. In all patients, fasting plasma glucose ( FPG) and fasting serum insulin( FIN) were determined and the insulin sensitively index (ISI) were calculated after admission and were repeated during 2-3 weeks after stroke onset. Results:(1)Patients with ischemic stroke had a significantly higher release of the NSE compared with the controlled subjects and Patients in compensatory hyperglycemia had more serious damage than those in normoglycemia. ( 2 ) LSI in stroke patient was significantly lower than that in controlled group and patients in compensatory hyperglycemia had the lowest ISI among these groups, indicating the presence of insulin rsistance in patients with cerebral infraction. There were also significant difference in FINS and ISI between the compensatory hyperglycemia patients and the normoglycemia not only in acute stage but also during 2-3 weeks after stroke onset. (3)In acute stage in compensatory hyperglycemia, the area under the plasma NSE concentraion curve was significantly correlated with the level of empty stomach glucose but had no correlation with the FINS or ISI. Conclusions: IR is the risk factor of the nonlacunar infarction but has limited influence on the ischemic damage and hyperglycemia maybe enhances the ischemic lesion.