MODULATION OF CEREBRAL ELECTROLYTE STATUS, LACTATE DEHYDROGENASE AND ACETYLCHOLINESTERASE ACTIVITIES BY KOLAVIRON FOLLOWING ISCHEMIA AND REPERFUSION INJURY

Abstract

Since neurochemical and electrolyte imbalances are important features in the pathophysiology of cerebral ischemia and reperfusion, the present study was carried out to investigate the modulation of cerebral electrolyte status and neurochemical activity by kolaviron following cerebral ischemia/reperfusion (I/R) injury. Ischemia was induced by ligation of the bilateral common carotid arteries for 30 min and followed by 4 h of reperfusion. Forty eight adult male Wistar rats were divided into the following groups: control group (sham), I/R group, kolaviron pretreated I/R group and kolaviron pretreated group. Kolaviron (100 mg/kg body weight and 200 mg/kg body weight) was administered orally to treated animals 1 hr before ischemia. After reperfusion, animals were evaluated for neurological defect using the initiation of walking, turning in the alley and beam balance tests. Animals were sacrificed and electrolyte levels and the activities of acetyl cholinesterase and lactate dehydrogenase were evaluated in the cortex and striatum of the brains of animals. The results revealed that I/R caused perturbations in Ca2+, Mg2+, K+ and Na+ ion levels as well as decreased activity of acetylcholinesterase and increased activity of lactate dehydrogenase in the cortex and striatum coupled with neurobehavioral deficit in experimental animals. Kolaviron, at both dosages significantly ameliorated I/R induced electrolyte imbalance, neurobiochemical changes and neurobehavioral deficits in rats. The results indicated that kolaviron is a potential therapeutic agent for ischemic disorders.