Duckrow R B, Beard D C, Brennan R W
Stroke. 1987 Jan-Feb;18(1):52-8. doi: 10.1161/01.str.18.1.52.
The presence of hyperglycemia prior to stroke or cardiac arrest can increase neuronal damage caused by brain ischemia. Acute hyperglycemia shows this effect in animal models of stroke. However, chronic hyperglycemia and chronic hyperglycemia with additional acute elevation of blood glucose are more common premorbid states for stroke patients. The effect of chronic hyperglycemia on regional cerebral blood flow (rCBF) is unclear but blood flow changes may play a role in this ischemic cell damage. We measured rCBF in awake restrained rats that had chronic hyperglycemia induced by treatment with streptozotocin. This was compared to that measured in rats made acutely hyperglycemic by injecting glucose into the peritoneal space. rCBF was measured in 17 brain regions using [14C]iodoantipyrine. During chronic hyperglycemia, when plasma glucose was 29 microns/ml, rCBF was decreased and a regional distribution of this effect was noted; 9 hindbrain regions showed a mean flow decrease of 14% while forebrain regions demonstrated less flow reduction. Acute elevation of plasma glucose during normoglycemia or superimposed on chronic hyperglycemia produced flow reductions of 7% for each 10 microns/ml increment in plasma glucose up to 60 microns/ml. Both chronic and acute hyperglycemia are associated with decreased rCBF and the mechanism for this effect does not appear to adapt to chronic hyperglycemia.
中风或心脏骤停前出现高血糖会增加脑缺血所致的神经元损伤。急性高血糖在中风动物模型中显示出这种作用。然而，慢性高血糖以及伴有血糖急性升高的慢性高血糖是中风患者更常见的病前状态。慢性高血糖对局部脑血流（rCBF）的影响尚不清楚，但血流变化可能在这种缺血性细胞损伤中起作用。我们测量了用链脲佐菌素诱导产生慢性高血糖的清醒束缚大鼠的rCBF。并将其与通过向腹腔注射葡萄糖使大鼠急性高血糖时所测得的rCBF进行比较。使用[¹⁴C]碘安替比林在17个脑区测量rCBF。在慢性高血糖期间，当血浆葡萄糖为29微摩尔/毫升时，rCBF降低，且注意到这种影响存在区域分布；9个后脑区域平均血流减少14%，而前脑区域血流减少较少。在正常血糖期间或叠加在慢性高血糖之上使血浆葡萄糖急性升高时，血浆葡萄糖每增加10微摩尔/毫升（直至60微摩尔/毫升），血流减少7%。慢性和急性高血糖均与rCBF降低有关，且这种作用机制似乎并不适应慢性高血糖。
