Jenkins L W, Lyeth B G, Lewelt W, Moszynski K, Dewitt D S, Balster R L, Miller L P, Clifton G L, Young H F, Hayes R L
Department of Anesthesiology, Medical College of Virginia, Richmond.
J Neurotrauma. 1988;5(4):275-87. doi: 10.1089/neu.1988.5.275.
Fasted Wistar rats were given a mild level of traumatic brain injury (TBI) and then subjected to 6 min of transient forebrain ischemia 24 h posttrauma. One group was given simultaneous 1 mg/kg scopolamine and 4 mg/kg phencyclidine intraperitoneally (IP) 15 min before trauma and another group an equal volume of plasmalyte A solution. After 7 days of postinjury survival, placebo-treated rats demonstrated increased posttraumatic vulnerability to secondary ischemic CA1 neuronal death even 24 h after trauma. This finding confirmed that increased posttraumatic ischemic vulnerability persists for at least 24 h even following mild trauma. Combined muscarinic receptor and N-methyl-D-aspartate (NMDA) receptor coupled ion channel blockade given and present during the mild TBI statistically attenuated this enhanced secondary ischemic CA1 neuronal death and thus posttraumatic increased ischemic vulnerability. Placebo-treated rats had 335.3 +/- 93.6 CA1 neurons/10(6) microns 2 and drug-treated rats had 844.8 +/- 184.9 CA1 neurons/10(6) microns 2. This result suggests that muscarinic and/or NMDA receptor-mediated events confined to TBI and the early posttraumatic period are in part responsible for the phenomenon of increased posttraumatic ischemic vulnerability.
对禁食的Wistar大鼠造成轻度创伤性脑损伤（TBI），然后在创伤后24小时使其经历6分钟的短暂性前脑缺血。一组在创伤前15分钟腹腔注射（IP）1毫克/千克东莨菪碱和4毫克/千克苯环利定，另一组注射等量的血浆代用品A溶液。伤后存活7天后，接受安慰剂治疗的大鼠即使在创伤后24小时，创伤后对继发性缺血性CA1神经元死亡的易感性也增加。这一发现证实，即使是轻度创伤后，创伤后缺血易感性增加至少持续24小时。在轻度TBI期间给予并存在的毒蕈碱受体和N-甲基-D-天冬氨酸（NMDA）受体偶联离子通道联合阻断在统计学上减弱了这种增强的继发性缺血性CA1神经元死亡，从而减弱了创伤后增加的缺血易感性。接受安慰剂治疗的大鼠每10⁶微米²有335.3±93.6个CA1神经元，接受药物治疗的大鼠每10⁶微米²有844.8±184.9个CA1神经元。这一结果表明，局限于TBI和创伤后早期的毒蕈碱和/或NMDA受体介导的事件部分导致了创伤后缺血易感性增加的现象。
