Plum F
Neurology. 1983 Feb;33(2):222-33. doi: 10.1212/wnl.33.2.222.
Improved treatment of associated cardiovascular and hematogenous abnormalities has favorably influenced the incidence and outcome of cerebral vascular disease during the past 25 years. Strong evidence now indicates that attention to the carbohydrate content of the brain also may influence outcome from brain ischemia. With brain lactate levels above approximately 16 mmol per kilogram, ischemia produces tissue infarction; ie, the lesion includes astrocytic and endothelial necrosis as well as neuronal death. We find that equal degrees of ischemia accompanied by lower tissue lactate values produce only selective neuronal damage in predictably vulnerable areas; astrocytes and endothelia are spared and extracellular or progressive postischemic cerebral edema fails to develop. The findings suggest that astrocytes can function to defend brain tissue against the damaging effects of acute anoxia but that during such conditions, they are potentially vulnerable to high tissue lactate levels. Initial clinical evidence suggests that scrupulous attention to blood sugar may reduce the risk of human cerebral infarction after ischemia.
在过去25年中，对相关心血管和血源性异常的治疗改善，对脑血管疾病的发病率和转归产生了有利影响。现在有力的证据表明，关注脑内碳水化合物含量也可能影响脑缺血的转归。当脑乳酸水平高于约每千克16毫摩尔时，缺血会导致组织梗死；也就是说，病变包括星形细胞和内皮细胞坏死以及神经元死亡。我们发现，同等程度的缺血伴有较低的组织乳酸值时，只会在可预测的易损区域产生选择性神经元损伤；星形细胞和内皮细胞未受影响，细胞外或缺血后进行性脑水肿也未发生。这些发现表明，星形细胞可以起到保护脑组织免受急性缺氧损伤的作用，但在这种情况下，它们可能易受高组织乳酸水平的影响。初步临床证据表明，严格关注血糖可能会降低人类缺血后脑梗死的风险。
