REGIONAL BRAIN SODIUM, POTASSIUM, AND WATER CHANGES IN THE RAT MIDDLE CEREBRAL-ARTERY OCCLUSION MODEL OF ISCHEMIA
REGIONAL BRAIN SODIUM, POTASSIUM, AND WATER CHANGES IN THE RAT MIDDLE CEREBRAL-ARTERY OCCLUSION MODEL OF ISCHEMIA
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DOI：
10.1161/01.str.18.4.751
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发表时间：
1987-07-01
期刊：
影响因子：
8.3
通讯作者：
FLAMM, ES
中科院分区：
文献类型：
--
作者：
YOUNG, W;RAPPAPORT, ZH;FLAMM, ES
大鼠大脑中动脉闭塞（MCAo）在梨状和额顶叶皮层产生梗死，并延伸到外侧基底节区和副矢状皮层。我们通过测量湿重和干重来估计组织水的浓度，并通过原子吸收光谱测定大鼠大脑这些区域的Na和K浓度。在MCAo和假MCAo后2、4和24小时对组织样本进行分析，并与未手术大鼠的正常值进行比较。在梨状区和额顶区，MCAo后2小时H2O浓度分别比正常高34.7%和7%，24小时H2O浓度分别比正常高89%和94%。这些地区的钠浓度在2小时内分别比正常高73%和37%，在24小时内分别比正常高281%和330%。K浓度直到4小时才发生变化，但在24小时时降至正常浓度的62%和34%。如此大的离子位移表明严重的组织破坏。在副矢状面皮层和基底节区，离子和水分的变化较小，直到MCAo后24小时才变得明显。钠进入梗死部位的速率在0-2小时最大，而钾的损失率在2 - 4小时达到峰值。钠内流和钾外排的差异导致净离子位移与水分进入高度相关，相关系数为0.992 (p < 0.001)，斜率表明每145 .mu有1 ml水进入组织。离子的摩尔。这些结果强烈提示净离子转移引起局部脑缺血的早期水肿。为了解释钠离子获得比钾离子损失的优势，我们拒绝了血脑屏障钠离子通透性选择性增加的假设，而是提出缺血神经元释放的K离子的胶质缓冲降低了MCAo后最初2-4小时内钾离子清除的驱动力。
Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the pyriform and frontoparietal cortex, extending into the lateral basal ganglia and parasagittal cortex. We estimated tissue H2O concentrations from wet and dry weight measurements and determined Na and K concentrations by atomic absorption spectroscopy in these areas of rat brains. Tissue samples were analyzed at 2, 4, and 24 hours after MCAo and sham MCAo, compared with normal values measured in unoperated rats. In the pyriform and frontoparietal areas, H2O concentrations increased to 34 and 7% greater than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na concentrations rose in these areas to 73 and 37% greater than normal by 2 hours, and 281 and 330% by 24 hours. K concentrations did not change until 4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such large ion shifts indicate severe tissue destruction. In the parasagittal cortex and basal ganglia areas, the ion and water changes were smaller and did not become significant until 24 hours after MCAo. Rates of Na entry into the infarct site were greatest at 0-2 hours, while the rates of K loss peaked later, between 2 and 4 hours. The difference in Na influx and K efflux resulted in net ion shifts that correlated highly with water entry, yielding a correlation coefficient of 0.992 (p < 0.001) and a slope indicating that 1 ml of water entered the tissue with each 145 .mu.moles of ions. These findings strongly suggest that net ion shifts cause the early edema of regional brain ischemia. To explain the dominance of Na gain over K loss, we reject the hypothesis of a selective increase of blood-brain barrier Na permeability and propose instead that glial buffering of K ions released by ischemic neurons reduced the driving force for K clearance during the first 2-4 hours after MCAo.