MacMillan V, Shankaran R
Brain Res. 1984 Jun 11;303(1):125-32. doi: 10.1016/0006-8993(84)90219-1.
In this study the cerebral Na+, K+-ATPase activity as well as selected parameters of oxidative metabolism and electrophysiological function were assessed in normoglycemic and hyperglycemic rats which were exposed to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. In hyperglycemic animals 0.5 h of ischemia was associated with massive accumulation of lactate (34 mumol X g-1) and enhanced Na+, K+-ATPase activity (116% control), whereas normoglycemic animals showed more moderate lactate accumulation (17 mumol X g-1) and normal Na+, K+-ATPase activity (102% control). In normoglycemic animals release of the carotid clamps and recirculation for 0.5-1.5 h was associated with a normalization of the lactate levels and a decrease in Na+, K+-ATPase activity (68-72% control). Restituted hyperglycemic animals showed metabolic changes which seemed related to the blood pressure, with hypotensive hyperglycemic animals showing continuing massive lactacidosis (30-35 mumol X g-1) and enhanced Na+, K+-ATPase activity (108-110% control), whereas normotensive hyperglycemic animals showed progressive decreases in lactate level (14-20 mumol X g-1) and normal or mildly suppressed Na+, K+-ATPase activity (88-97% control). These patterns of change suggest that the reperfusion of the post-ischemic hyperglycemic-hyperlactacidotic brain was inadequate or non-homogeneous.
在本研究中，对正常血糖和高血糖大鼠的脑钠钾ATP酶活性以及氧化代谢和电生理功能的选定参数进行了评估，这些大鼠暴露于通过椎动脉电灼和颈动脉可逆性闭塞产生的缺血状态。在高血糖动物中，0.5小时的缺血与乳酸大量积累（34μmol·g-1）和钠钾ATP酶活性增强（为对照的116%）相关，而正常血糖动物的乳酸积累较为适度（17μmol·g-1）且钠钾ATP酶活性正常（为对照的102%）。在正常血糖动物中，松开颈动脉夹并再灌注0.5 - 1.5小时与乳酸水平正常化和钠钾ATP酶活性降低（为对照的68 - 72%）相关。恢复后的高血糖动物表现出似乎与血压相关的代谢变化，低血压高血糖动物持续出现大量乳酸性酸中毒（30 - 35μmol·g-1）且钠钾ATP酶活性增强（为对照的108 - 110%），而正常血压高血糖动物的乳酸水平逐渐降低（14 - 20μmol·g-1）且钠钾ATP酶活性正常或轻度受抑（为对照的88 - 97%）。这些变化模式表明，缺血后高血糖 - 高乳酸血症脑的再灌注不充分或不均匀。
