Duckrow R B, Beard D C, Brennan R W
Ann Neurol. 1985 Mar;17(3):267-72. doi: 10.1002/ana.410170308.
The presence of hyperglycemia before brain ischemia increases stroke-related morbidity and mortality in experimental animals and humans. However, little is known of the effect of hyperglycemia on regional cerebral blood flow (rCBF). Acute hyperglycemia was induced in awake but restrained rats by intraperitoneal injection of 50% D-glucose. Regional flow was determined using [14C]iodoantipyrine and quantitative autoradiography. Elevation of plasma glucose from 11 to 39 mM was associated with a 24% reduction in rCBF when compared with controls that received normal saline. Intraperitoneal D-mannitol produced an elevation of plasma osmolality equivalent to that observed with glucose. However, rCBF was only reduced by 10%. Hyperglycemia appears to produce a global decrease in rCBF in awake rats that cannot be completely explained by the attendant increase in plasma osmolality. If a similar influence is present during brain ischemia, hyperglycemia could extend areas of critical flow limitation.
脑缺血前存在高血糖会增加实验动物和人类与中风相关的发病率和死亡率。然而，关于高血糖对局部脑血流量（rCBF）的影响却知之甚少。通过腹腔注射50% D-葡萄糖在清醒但受束缚的大鼠中诱导急性高血糖。使用[14C]碘安替比林和定量放射自显影术测定局部血流量。与接受生理盐水的对照组相比，血浆葡萄糖从11 mM升高至39 mM时，rCBF降低了24%。腹腔注射D-甘露醇使血浆渗透压升高至与葡萄糖所观察到的相当水平。然而，rCBF仅降低了10%。高血糖似乎会使清醒大鼠的rCBF整体下降，而血浆渗透压随之升高并不能完全解释这一现象。如果在脑缺血期间存在类似影响，高血糖可能会扩大临界血流受限区域。
