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pubmed-article:8000978pubmed:abstractTextRecent brain research proposes that, during ischemia, synaptically released excitatory amino acid neurotransmitters accumulate at toxic concentrations with ensuing neuronal death. Their action is mediated by the receptor subtype N-methyl-D-aspartate (NMDA). The protective effect of NMDA receptor blockade with intrathecal MgSO4 and MK-801 was investigated during spinal cord ischemia induced by aortic occlusion of 12 minutes. Male Sprague-Dawley rats, 250-300g, underwent intrathecal administration of 20 microL of normal saline (SA n = 16), MgSO4 1M (MG n = 16), or MK-801, 25 mM solutions (MK n = 16) in a randomized order. After 2 hours, the animals underwent occlusion of the thoracic aorta and subclavian arteries for 12 min. An additional control group (CO n = 16) underwent occlusion for 12 minutes, without intrathecal injection. The animals were scored according to their functional performance (LS = lesion score) each day for four days by a blinded observer. Mean LS were calculated for each group at a given day. Treatment and control groups were not different at day 1 (P = 0.302). Group MG was improved from groups SA (P = < 0.0039) and CO (P = < 0.0048) at day 4. This study demonstrates that although intrathecal NMDA receptor blockade with MgSO4 or MK-801 does not prevent paraplegia due to spinal cord ischemia in the rat, it could however influence the rate of recovery after ischemic injury.lld:pubmed
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pubmed-article:8000978pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:8000978pubmed:articleTitleNMDA receptor blockade and spinal cord ischemia due to aortic crossclamping in the rat model.lld:pubmed
pubmed-article:8000978pubmed:affiliationDepartment of Thoracic and Cardiothoracic Surgery, University of New Mexico, Albuquerque 87131.lld:pubmed
pubmed-article:8000978pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8000978pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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