Prasad M R, Dhillon H S, Carbary T, Dempsey R J, Scheff S W
Department of Surgery, University of Kentucky Chandler Medical Center, Lexington 40536-0084.
J Neurochem. 1994 Aug;63(2):773-6. doi: 10.1046/j.1471-4159.1994.63020773.x.
Regional levels of lactate and inositol 1,4,5-trisphosphate (IP3), a cellular second messenger of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue lactate concentrations were significantly elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres. By 20 min postinjury, lactate concentrations were elevated only in the cortices and hippocampus of the ipsilateral hemisphere. Whereas the IP3 concentrations were elevated in the hippocampi of the ipsilateral and contralateral hemisphere and in the cortex of ipsilateral hemisphere at 5 min postinjury, no elevation in these sites was found at 20 min postinjury. Histologic analysis revealed neuronal damage in the cortex and CA3 regions of hippocampus ipsilateral to the injury at 24 h postinjury. The present results suggest activation of the phosphoinositide signal transduction pathway at the onset of injury and of a possible requirement of early persistent metabolic dysfunction (> 20 min) such as the lactate accumulation in the delayed neuronal damage.
在大鼠进行侧方液压脑损伤（FP）后，测量了局部乳酸和肌醇1,4,5-三磷酸（IP3，兴奋性神经递质系统的一种细胞第二信使）的水平。损伤后5分钟，同侧和对侧半球的皮质和海马组织中的乳酸浓度显著升高。损伤后20分钟，乳酸浓度仅在同侧半球的皮质和海马中升高。损伤后5分钟时，同侧和对侧半球的海马以及同侧半球皮质中的IP3浓度升高，但在损伤后20分钟时，这些部位未发现升高。组织学分析显示，损伤后24小时，损伤同侧海马的皮质和CA3区存在神经元损伤。目前的结果表明，在损伤开始时磷酸肌醇信号转导通路被激活，并且可能需要早期持续的代谢功能障碍（>20分钟），例如延迟性神经元损伤中的乳酸积累。
