MacMillan V
J Cereb Blood Flow Metab. 1982 Dec;2(4):457-65. doi: 10.1038/jcbfm.1982.52.
This study documents the Na+,K+-ATPase activity as well as selected parameters of oxidative metabolism and electrophysiological function in rat brain exposed to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. During a 0.5-h ischemic exposure in which the electroencephalograph (EEG) was abolished and energy metabolism severly compromised the Na+,K+-ATPase showed a capability for enhanced activity (120-140% of control). On recirculation, the Na+,K+-ATPase activity showed a phasic pattern, which was characterized by normal values at 0.25-2 h, increased values (115-125% of control) at 3-24 h, and, finally, normal values at 72 h of recirculation, respectively. The maintenance of Na+,K+-ATPase integrity was correlated with a gradual return of EEG activity and virtually complete restitution of the cerebral energy state during the 72 h of recirculation. Measurements of thiobarbituric acid reactive material and water soluble antioxidant during ischemia and recirculation gave no evidence of the presence of significant free radical lipid peroxidation in this model. It is concluded that Na+,K+-ATPase and its associated membrane lipids are not irreversibly damaged by ischemia in which the tissue lactacidosis is limited to less than 20 mumol g-1.
本研究记录了大鼠大脑在接受椎动脉电灼和颈动脉可逆性闭塞所产生的缺血时，钠钾ATP酶的活性以及氧化代谢和电生理功能的选定参数。在0.5小时的缺血暴露期间，脑电图（EEG）消失，能量代谢严重受损，此时钠钾ATP酶显示出活性增强的能力（为对照值的120%-140%）。再灌注时，钠钾ATP酶活性呈现出阶段性模式，其特征分别为再灌注0.25-2小时时活性正常，3-24小时时活性升高（为对照值的115%-125%），最后在再灌注72小时时活性恢复正常。钠钾ATP酶完整性的维持与脑电图活动的逐渐恢复以及再灌注72小时期间大脑能量状态的几乎完全恢复相关。在缺血和再灌注期间对硫代巴比妥酸反应性物质和水溶性抗氧化剂的测量未发现该模型中存在明显的自由基脂质过氧化现象。得出的结论是，在组织乳酸酸中毒限于低于20μmol g-1的缺血情况下，钠钾ATP酶及其相关膜脂不会受到不可逆损伤。
