Duckrow R B, Bryan R M
J Neurochem. 1987 Mar;48(3):989-93. doi: 10.1111/j.1471-4159.1987.tb05614.x.
Previous data indicate that regional cerebral blood flow (rCBF) decreases during acute and chronic hyperglycemia. To test the hypothesis that the decrease in rCBF is secondary to a decrease in cerebral metabolic rate, the rate of regional cerebral glucose utilization (rCMRgl) was measured in awake-restrained rats during acute and chronic hyperglycemia. Acute hyperglycemia was produced by intraperitoneal injection of glucose, and chronic hyperglycemia was produced by treatment with streptozotocin. The rCMRgl was measured over a 10-min period using [6-14C]glucose. Glucose utilization was normal during acute hyperglycemia but decreased by 13% following 3 weeks of chronic hyperglycemia. The absence of a decrease in rCMRgl measured during acute hyperglycemia indicates that decreased rCBF cannot be explained by a change in the metabolic rate of the brain. The decrease in rCMRgl measured during chronic hyperglycemia does not necessarily indicate the presence of a drop in the metabolic rate of the brain because ketone bodies are available as an alternate fuel for oxidative metabolism. Therefore, it is unlikely that the decrease in rCMRgl measured during chronic hyperglycemia accounts for decreased rCBF.
先前的数据表明，在急性和慢性高血糖期间，局部脑血流量（rCBF）会降低。为了验证rCBF降低继发于脑代谢率降低这一假设，在清醒受限的大鼠急性和慢性高血糖期间测量了局部脑葡萄糖利用率（rCMRgl）。急性高血糖通过腹腔注射葡萄糖产生，慢性高血糖通过链脲佐菌素治疗产生。使用[6-14C]葡萄糖在10分钟内测量rCMRgl。急性高血糖期间葡萄糖利用率正常，但慢性高血糖3周后降低了13%。急性高血糖期间测量的rCMRgl没有降低，这表明rCBF降低不能用大脑代谢率的变化来解释。慢性高血糖期间测量的rCMRgl降低不一定表明大脑代谢率下降，因为酮体可作为氧化代谢的替代燃料。因此，慢性高血糖期间测量的rCMRgl降低不太可能是rCBF降低的原因。
