Preconditioning with ouabain reduces the neurological deficit in rats caused by compression-induced cerebral ischemia

Abstract

Ischaemic brain damage is a major neurobiological and medical social problem, making experimental research of the pathogenesis of cerebral ischemia and the search for ways to minimize its consequences particularly relevant. The aim of the study was to determine the possibility of reducing the neurological deficit and functional limb asymmetry in laboratory rats through ischaemic tolerance using ouabain, a Na+/K+- ATPase inhibitor. Materials and methods. Cerebral ischemia was modeled using 20-minute focal compression of the left sensorimotor cortex in the rat brain. To induce tolerance, laboratory animals were given a single intravenous injection of 0.7 mg/kg of the Na+/K+-ATPase inhibitor ouabain 24 or 72 hours before the ischaemic event. Functional impairment was assessed with tests for neurological deficits in the limbs and a test for forelimb performance in laboratory animals. Results. Preliminary ouabain administration prevented the development of functional impairment due to compression-induced ischemia of the sensorimotor cortex, with a decrease in limb asymmetry and the severity of motor dysfunction. Conclusion. In animals, pharmacological preconditioning with ouabain increases the brain's resistance to subsequent compression-induced ischemia, preventing functional asymmetry and improving both right and left limb function. The obtained data expand the possibilities of using Na+/K+-ATPase inhibitors to treat cerebral ischemia.

Keywords

• compression-induced ischemia
• ischaemic tolerance
• functional deficit