Cerebral Na+,K+-ATPase activity during exposure to and recovery from acute ischemia.

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.