Matsumoto M, Iida Y, Sakabe T, Sano T, Ishikawa T, Nakakimura K
Department of Anesthesiology-Resuscitology, Yamaguchi University, School of Medicine, Japan.
Anesthesiology. 1997 May;86(5):1120-7. doi: 10.1097/00000542-199705000-00016.
Controversy exists over the efficacy of different methods for protecting the spinal cord against experimental ischemic injury. Therefore, the authors compared the protective effects of thiopental with those of hypothermia (35 degrees C and 32 degrees C) on hindlimb motor functions and histopathology after transient spinal cord ischemia.
Twenty-seven New Zealand white rabbits were assigned to one of the four groups: a thiopental-normothermia group (burst-suppression dose of thiopental; esophageal temperature = 38 degrees C; n = 7), a halothane-mild hypothermia group (halothane, 1%; esophageal temperature = 35 degrees C; n = 7), a halothane-moderate hypothermia group (halothane, 1%; esophageal temperature = 32 degrees C; n = 6), and a halothane-normothermia group (halothane, 1%; esophageal temperature = 38 degrees C; n = 7). The animals were then subjected to 20 min of spinal cord ischemia produced by occlusion of the aorta distal to the origin of left renal artery. Hindlimb motor function was observed for 48 h after reperfusion. Histopathology of the lumbar spinal cord also was examined.
All animals in the halothane-mild hypothermia and halothane-moderate hypothermia groups were neurologically normal 48 h after ischemia. There was no statistical difference in the final neurologic status and histopathology between the thiopental-normothermia and halothane-normothermia groups. However, the final neurologic status and histopathology in both groups were worse than in the halothane-mild hypothermia or halothane-moderate hypothermia groups. There was a strong correlation between the final neurologic status and the numbers of normal neurons in the anterior spinal cord.
These results suggest that mild and moderate hypothermia protects against ischemic spinal cord injury in rabbits, and a burst-suppression dose of thiopental does not offer any advantage over halothane.
不同方法保护脊髓免受实验性缺血损伤的疗效存在争议。因此,作者比较了硫喷妥钠与低温(35摄氏度和32摄氏度)对短暂性脊髓缺血后后肢运动功能和组织病理学的保护作用。
将27只新西兰白兔分为四组之一:硫喷妥钠-正常体温组(硫喷妥钠爆发抑制剂量;食管温度=38摄氏度;n=7)、氟烷-轻度低温组(氟烷,1%;食管温度=35摄氏度;n=7)、氟烷-中度低温组(氟烷,1%;食管温度=32摄氏度;n=6)和氟烷-正常体温组(氟烷,1%;食管温度=38摄氏度;n=7)。然后对动物进行左肾动脉起源远端主动脉闭塞导致的20分钟脊髓缺血。再灌注后观察后肢运动功能48小时。还检查了腰段脊髓的组织病理学。
氟烷-轻度低温组和氟烷-中度低温组的所有动物在缺血48小时后神经功能正常。硫喷妥钠-正常体温组和氟烷-正常体温组之间的最终神经状态和组织病理学无统计学差异。然而,两组的最终神经状态和组织病理学均比氟烷-轻度低温组或氟烷-中度低温组差。最终神经状态与脊髓前角正常神经元数量之间存在强相关性。
这些结果表明,轻度和中度低温可保护兔脊髓免受缺血性损伤,硫喷妥钠的爆发抑制剂量并不比氟烷有任何优势。