全脑缺血期间的氢离子缓冲
Hydrogen ion buffering during complete brain ischemia.
作者信息
Kraig R P, Pulsinelli W A, Plum F
出版信息
Brain Res. 1985 Sep 9;342(2):281-90. doi: 10.1016/0006-8993(85)91127-8.
As a first step to quantify [H+] changes in brain during ischemia we used H+-selective microelectrodes and enzyme fluorometric techniques to describe the relationship between interstitial [H+] ([H+]o) and peak tissue lactate after cardiac arrest. We found a step function relationship between [H+]o and tissue lactate rather than the linear titration expected in a homogeneous protein solution. Within a blood glucose range from 3-7 mM, brain lactate rose from 8-13 mmol/kg along with a rise in [H+]o of 99 +/- 6 nM(0.44 +/- 0.02 pH). At higher blood glucose levels (17-80 mM), brain lactate accumulated to levels of 16-31 mmol/kg; concurrently [H+]o rose by 608 +/- 16 nM (1.07 +/- 0.02 pH). The unchanging level of [H+]o between 8-13 and 16-31 mmol/kg lactate implies that [H+]o is at a steady-state, but not equilibrium with respect to [H+] in other brain compartments. We propose that ion-transport characteristics of astroglia account for the observed relationship of [H+]o to tissue lactate during complete ischemia and suggest that brain infarction develops after plasma membranes in brain cells can no longer transport ions to regulate [H+].
作为量化缺血期间大脑中[H⁺]变化的第一步，我们使用H⁺选择性微电极和酶荧光技术来描述心脏骤停后间质H⁺与组织乳酸峰值之间的关系。我们发现[H⁺]o与组织乳酸之间呈阶跃函数关系，而非均匀蛋白质溶液中预期的线性滴定关系。在血糖范围为3 - 7 mM时，脑乳酸从8 - 13 mmol/kg升高，同时[H⁺]o升高99±6 nM(0.44±0.02 pH)。在较高血糖水平(17 - 80 mM)时，脑乳酸积累至16 - 31 mmol/kg；同时[H⁺]o升高608±16 nM(1.07±0.02 pH)。在乳酸水平为8 - 13 mmol/kg和16 - 31 mmol/kg之间[H⁺]o不变，这意味着[H⁺]o处于稳态，但相对于其他脑区室中的[H⁺]并非平衡状态。我们提出星形胶质细胞的离子转运特性解释了完全缺血期间观察到的[H⁺]o与组织乳酸之间的关系，并表明在脑细胞中的质膜不再能够转运离子以调节[H⁺]后会发生脑梗死。
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