Alterations in Na(+)-K(+)-ATPase activity and beta-endorphin content in acute ischemic brain with and without naloxone treatment.

The Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase) activity and beta-endorphin immunoreactivity were determined in rat brain at the acute stage of ischemia produced by unilateral occlusion of the middle cerebral artery (MCA). The effect of pretreatment with naloxone on these activities was also evaluated in the same model. After MCA occlusion, Na(+)-K(+)-ATPase activity was promptly reduced in the ischemic hemisphere and remained at a lower level than in the contralateral hemisphere during 90 minutes of ischemia. A single intraperitoneal 0.5-mg injection of naloxone prior to MCA occlusion attenuated the inactivation. On the other hand, beta-endorphin immunoreactivity was significantly increased following ischemia. The increase was marked in the ischemic hemisphere and was also observed in the contralateral hemisphere; this increase was not affected by the administration of naloxone. These results indicate the possibility that naloxone contributes to protecting the brain from ischemia through stabilizing the cellular membrane. The possible mechanism by which naloxone attenuates the inactivation of Na(+)-K(+)-ATPase in the ischemic brain is discussed in view of alterations of the central beta-endorphin system during ischemia.