Evans D E, Catron P W, McDermott J J, Thomas L B, Kobrine A I, Flynn E T
Diving Medicine Department, Naval Medical Research Institute, Bethesda, Maryland.
J Neurosurg. 1989 Jan;70(1):97-102. doi: 10.3171/jns.1989.70.1.0097.
To investigate possible approaches to the treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, somatosensory evoked potentials (SEP's) were measured after cerebral air embolism in the anesthetized cat. Air was introduced into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to approximately 10% or less of baseline values. Either a saline or lidocaine infusion was begun 5 minutes after inducing cerebral ischemia. In the saline-treated group, SEP amplitude was reduced to 6.7% +/- 1.6% (mean +/- standard error of the mean) of baseline, with a return to 32.6% +/- 4.7% of baseline over a 2-hour period. In the lidocaine-treated group, SEP amplitude was reduced to 5.9% +/- 1.5%, with a return to 77.3% +/- 6.2% over a 2-hour period. The results suggest that lidocaine administration facilitates the return of neural function after acute cerebral ischemia induced by air embolism.
为了研究治疗空气栓塞及其他形式急性脑缺血所致神经损伤的可能方法，在麻醉猫发生脑空气栓塞后测量体感诱发电位（SEP）。以0.08毫升的增量将空气注入颈动脉，直至SEP幅度降低至基线值的约10%或更低。在诱导脑缺血5分钟后开始输注生理盐水或利多卡因。在生理盐水治疗组中，SEP幅度降低至基线的6.7%±1.6%（平均值±平均标准误差），并在2小时内恢复至基线的32.6%±4.7%。在利多卡因治疗组中，SEP幅度降低至5.9%±1.5%，并在2小时内恢复至77.3%±6.2%。结果表明，给予利多卡因有助于空气栓塞所致急性脑缺血后神经功能的恢复。
