Improvement of 2-Vessel Occlusion Cerebral Ischaemia/Reperfusion-Induced Corticostriatal Electrolyte and Redox Imbalance, Lactic Acidosis and Modified Acetylcholinesterase Activity by Kolaviron Correlates with Reduction in Neurobehavioural Deficits.

Background: Disruption of electrolyte, redox and neurochemical homeostasis alongside cellular energy crisis is a hallmark of cerebral ischaemia and reperfusion injury.

Purpose: This study investigated the effect of kolaviron (KV) on cortical and striatal cation imbalance, oxidative stress and neurochemical disturbances as well as neurobehavioural deficits in animals subjected to bilateral common carotid artery occlusion (BCCAO)-induced ischaemia/reperfusion injury.

Methods: KV was administered at a dose of 100 or 200 mg/kg to male Wistar rats 1 h before a 30 min BCCAO/4 h reperfusion (I/R). This was followed by neurobehavioral assessment and biochemical evaluations of cation levels, oxidative stress indicators, lactate dehydrogenase activity and acetylcholinesterase (AChE) activity in the brain of animals.

Conclusion: KV significantly restored altered cortical and striatal Ca, Na, K and Mg levels, ameliorated redox imbalance, lactic acidosis and modified AChE activity caused by I/R injury. The favourable neurobehavioural effects of KV correlated with biochemical outcomes. The pharmacological potential of KV in the treatment and management of ischemic stroke and allied pathological conditions via multiple targets (neurotransmitter metabolism, bioenergetic failure and ionic homeostasis) is highlighted by the study.