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Korean Journal of Anesthesiology 2002;42(5):660-666.
DOI: https://doi.org/10.4097/kjae.2002.42.5.660   
The Effects of Intravenous Ketamine on Neurologic Injury and Glutamate Receptor Gene Expression after Transient Spinal schemia in the Rat.
Jae Young Kwon, Young Chan Joo, Chul Hong Kim, Kyoung Hoon Kim, Hae Kyu Kim, Seong Wan Baik
Department of Anesthesiology, College of Medicine, Pusan National University, Busan, Korea. jykwon@pusan.ac.kr
Massive release of glutamate plays an important role in ischemic neuronal injury, and modification of this process may provide neuroprotection. We studied the protective effects of the N- methyl-D-aspartate receptor antagonist ketamine on hind limb motor function and glutamate receptor of gene expression in an experimental model of spinal cord ischemia.
Transient spinal cord ischemia was induced by 15 min of thoracic aortic occlusion in 24 anesthetized Sprague-Dawly rats. Rats were randomly assigned to one of three treatment groups (n = 8 each): C group, no intervention; K30 group, ketamine 30 mg/kg intravenously; or K50 group, ketamine 50 mg/kg intravenously. Normothermia (38degreesC) was maintained during ischemia. After spinal ischemia neurologic function was evaluated immediately and after 1, 2 and 3 hours. After 3 hours rats were euthanized and spinal cords were removed for the assay of NMDAR and mGluR5 mRNA.
Neurologic outcome was better in the K30 group than the C or K50 group (P < 0.05). The NMDAR mRNA expression of the K30 and K50 group were greater than those of the C group. The mGluR5 mRNA expression increased after spinal ischemia. There were no differences between groups.
In this study demonstrated that treatment with ketamine 30 mg/kg intravenously before ischemia increases tolerance of spinal cord motor neurons in a period of normothermic ischemia.
Key Words: Ketamine; glutamate receptor 5 mRNA; N-methyl-D-asparatate receptor; spinal cord ischemia


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