Neuroprotective effects of riluzole and ketamine during transient spinal cord ischemia in the rabbit

Background Massive release of central excitatory neurotransmitters is an im portant Initial step in ischemic neuronal injury, and modification of this process may provide neuroprotection, We studied the protective effects of t he voltage-dependent sodium channel antagonist riluzole and the N-methyl-D- aspartate receptor antagonist ketamine on hind limb motor function and hist opathologic outcome in an experimental model of spinal cord ischemia. Methods: Temporary spinal cord Ischemia was induced by 29 min of infrarenal balloon occlusion of the aorta in 60 anesthetized New Zealand white rabbit s. Animals were randomly assigned to one of four treatment groups (n = 15 e ach): group C, saline (control); group R, riluzole, 8 mg/kg intravenously; group K, ketamine, 55 mg/kg intravenously; group RK, riluzole and ketamine, After reperfusion, riluzole treatment was continued with intraperitoneal i nfusions, Normothermia (38 degreesC) was maintained during ischemia, and re ctal temperature was assessed before and after intraperitoneal infusions, N eurologic function, according to Tarlov's criteria, was evaluated every 24 h, and Infarction volume and. the number of eosinophilic neurons and viable motoneurons In the lumbosacral spinal cord was evaluated after 72 h Results: Neurologic outcome was better in groups it and RK than bl groups C and K. All animals in group C (100%) and all animals but one in group K (9 3%) were paraplegic 72 h after the ischemic insult versus 53% In group R an d 67% in group RK (P < 0.01 each). More viable motoneurons were present in groups R and RK than in controls (P < 0.05), Conclusions: The data indicate that treatment with riluzole can increase th e tolerance of spinal cord motoneurons to a period of normothermic ischemia , Intraischemic ketamine did not provide neuroprotection in this model.