ALCOHOL EXACERBATES BEHAVIORAL AND NEUROCHEMICAL EFFECTS OF RAT SPINAL-CORD TRAUMA
ALCOHOL EXACERBATES BEHAVIORAL AND NEUROCHEMICAL EFFECTS OF RAT SPINAL-CORD TRAUMA
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DOI：
10.1001/archneur.1992.00530350096025
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发表时间：
1992-11-01
影响因子：
--
通讯作者：
FADEN, AI
中科院分区：
文献类型：
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作者：
HALT, PS;SWANSON, RA;FADEN, AI
急性酒精中毒可能会加剧中枢神经系统创伤的后果，尽管机制尚不确定。观察急性乙醇处理对大鼠脊髓损伤后行为学和神经化学变化的影响。与生理盐水对照组相比，酒精治疗组的存活率降低，创伤后神经功能恶化。与对照组相比，酒精处理组大鼠的兴奋性氨基酸组织水平显著降低，而游离脂肪酸、血栓烷和乳酸水平显著升高。组织镁浓度因创伤而显著降低，在酒精处理的大鼠恢复较慢。在急性酒精中毒所致的脊髓损伤后，游离脂肪酸和血栓素的磷脂水解率增加，兴奋性氨基酸的释放增加，组织镁水平降低，都可能导致继发性组织损伤加重，神经功能恢复减慢。
Acute alcohol intoxication may exacerbate the consequences of central nervous system trauma, although the mechanism is uncertain. Effects of acute ethanol administration on behavioral and neurochemical changes were examined in rats after traumatic spinal cord injury. Survival rates were reduced and posttraumatic neurologic function worsened in ethanol-treated as compared with saline-treated controls. Ethanol-treated rats had significantly lower tissue levels of excitatory amino acids and higher levels of free fatty acids, thromboxane, and lactic acid than did controls. Tissue magnesium concentration was significantly reduced by trauma and recovered more slowly in ethanol-treated rats. Enhanced phospholipid hydrolysis with free fatty acid and thromboxane accumulation, increased release of excitatory amino acids, and decreased tissue magnesium levels may each serve to worsen secondary tissue damage and diminish neurologic recovery after spinal cord injury associated with acute alcohol intoxication.