Katsura K, Minamisawa H, Ekholm A, Folbergrová J, Siesjö B K
Laboratory for Experimental Brain Research, University Hospital of Lund, Sweden.
Brain Res. 1992 Sep 11;590(1-2):6-12. doi: 10.1016/0006-8993(92)91075-p.
The objective of this study was to assess the influence of temperature on the coupling among energy failure, depolarization, and ionic fluxes during anoxia. To that end, we induced anoxia by cardiac arrest in anesthetized rats maintained at a body temperature of either 34 degrees C or 40 degrees C, measured extracellular K+ concentration (K+e), and froze the neocortex through the exposed dura for measurements of phosphocreatine (PCr), creatine (Cr), ATP, ADP, and AMP, glucose, glycogen, pyruvate and lactate content after ischemic intervals of maximally 130 s. Free ADP (ADPf) concentrations were derived from the creatine kinase equilibrium. Hypothermia reduced the initial rate of rise in K+e, and delayed the terminal depolarization; however, both hypo- and hyperthermic animals showed massive loss of ion homeostasis at a K+e of 10-15 mM. The initial rate of rise in K+e did not correlate to changes in ATP, or ATP/ADPf ratio, suggesting that temperature changes per se may control the degree of activation of K+ conductances. The results clearly showed that, in both hyper- and hypothermic subjects, energy failure preceded the sudden activation of membrane conductances for ions. The results indicate that temperature primarily influences membrane permeability to ions like K+e (and Na+), and that cerebral energy state is secondarily affected. It is proposed that the higher rate of rise of K+e at high temperatures accelerates ATP hydrolysis primarily by enhancing metabolic rate in glial cells.
本研究的目的是评估温度对缺氧期间能量衰竭、去极化和离子通量之间耦合的影响。为此，我们通过心脏停搏在体温维持在34℃或40℃的麻醉大鼠中诱导缺氧，测量细胞外K⁺浓度（K⁺e），并通过暴露的硬脑膜冷冻新皮质，以测量在最长130秒的缺血间隔后的磷酸肌酸（PCr）、肌酸（Cr）、ATP、ADP和AMP、葡萄糖、糖原、丙酮酸和乳酸含量。游离ADP（ADPf）浓度由肌酸激酶平衡推导得出。低温降低了K⁺e的初始上升速率，并延迟了终末期去极化；然而，低温和高温动物在K⁺e为10 - 15 mM时均显示出离子稳态的大量丧失。K⁺e的初始上升速率与ATP或ATP/ADPf比值的变化无关，这表明温度变化本身可能控制K⁺电导的激活程度。结果清楚地表明，在高温和低温受试者中，能量衰竭都先于离子膜电导的突然激活。结果表明，温度主要影响膜对K⁺e（和Na⁺）等离子的通透性，其次才影响脑能量状态。有人提出，高温下K⁺e的较高上升速率主要通过提高神经胶质细胞的代谢率来加速ATP水解。
