Lucas L F, West C A, Rigor B M, Schurr A
Department of Anesthesiology, University of Louisville School of Medicine, KY 40292.
J Neurosci Methods. 1989 May;28(1-2):47-50. doi: 10.1016/0165-0270(89)90008-3.
The ability of the local anesthetics lidocaine, 2-chloroprocaine and cocaine to protect neuronal tissue against hypoxic damage was evaluated. Rat hippocampal slices were incubated with non-depressive doses of these agents 60 min prior to their exposure to 15 min hypoxia. The rate of recovery of synaptic function (evoked field potentials) following the hypoxic episode was used as an index of hypoxic damage. Slices treated with 0.1 mM of any of the three local anesthetics exhibited a significant increase in the recovery rate of synaptic function from hypoxia as compared to control, untreated slices. These results indicate that local anesthetics, by reducing neuronal sodium influx (and possibly its concomitant calcium influx) which occurs upon hypoxic depolarization, are able to prolong the hypoxic insult a cerebral tissue could tolerate.
评估了局部麻醉药利多卡因、2-氯普鲁卡因和可卡因保护神经元组织免受缺氧损伤的能力。在将大鼠海马切片暴露于15分钟缺氧环境前60分钟,用这些药物的非抑制剂量对其进行孵育。缺氧发作后突触功能(诱发场电位)的恢复率被用作缺氧损伤的指标。与未处理的对照切片相比,用0.1 mM这三种局部麻醉药中的任何一种处理的切片,其缺氧后突触功能的恢复率显著增加。这些结果表明,局部麻醉药通过减少缺氧去极化时发生的神经元钠内流(以及可能伴随的钙内流),能够延长脑组织所能耐受的缺氧损伤时间。