缺血预处理快速效应对兔急性缺血脊髓的保护作用

Protective effect of rapid ischemic preconditioning against spinal cord ischemic injury in rabbits

目的 :探讨缺血预处理快速相对兔腹主动脉短暂阻断致缺血脊髓的保护作用。方法 :36只雄性新西兰兔随机分成 3组 (n =12 ) :即缺血再灌注损伤组 (IR组 )、缺血预处理组 (IPC +IR组 )及假手术组 (Sham组 )。IR组阻闭兔腹主动脉肾下段 2 0min ,复制兔脊髓缺血损伤模型 ;IPC +IR组预先阻闭腹主动脉肾下段 6min ,再灌注 30min后再次阻闭腹主动脉肾下段 2 0min ;Sham组除不夹闭腹主动脉外 ,其余处理同IR组。再灌注后 8h、12h、2 4h和4 8h分别对动物神经功能评分 ,然后 ,处死动物取脊髓 (L5-7) ,分别行组织病理学观察及测定脊髓组织中Na+ ,K+ -ATP酶的活性。结果 :Sham组及IPC +IR组神经功能评分各时点均明显高于IR组 (P <0 0 1) ;Sham组及IPC +IR组脊髓前角正常神经细胞数明显多于IR组 (P <0 0 1) ;Sham组及IPC +IR组脊髓组织中Na+ ,K+ -ATP酶的活性明显高于IR组 (P <0 0 1)。结论 :缺血预处理快速相对兔急性缺血脊髓有显著的保护作用 ,这种保护作用可能与稳定Na+ ,K+

AIM: To evaluate the protective effect of rapid phase of ischemic preconditioning against spinal cord ischemic injury in rabbits. METHODS: Thirty six male New Zealands white rabbits were randomly assigned to 3 groups (12 in each group): ischemia and reperfusion injury group (IR group), ischemic preconditioning + IR group (IPC+IR group) and sham operation group (sham). In IR group, spinal cord ischemia was induced by an infrarenal aorta clamping for 20 min; The rabbits in IPC+IR group underwent a 6 min ischemic preconditioning followed by 30 min of reperfusion before the 20 min clamping; The rabbits in sham group underwent the same procedures as the IR group except for infrarental aortic unclamping. Neurologic status was scored at 8, 12, 24 and 48 h after reperfusion. All animals were sacrificed at 48 h after reperfusion and the spinal cords (L_(5-7)) were removed for histopathologic study and determination of the activity of Na^+, K^+-ATPase. RESULTS: The neurologic function scores in sham group and IPC+IR group at each observation interval were higher than those in IR group (P<0.01). Compared to IR group, there were more normal neurons in anterior horn of spinal cord in sham group and IPC+IR group (P<0.01); the activity of Na^+, K^+-ATPase in sham group and IPC+IR group were higher than those in IR group (P<0.01). CONCLUSION: The rapid phase of ischemic preconditioning has a protective effect against spinal cord ischemic injury in rabbits, and this neuroprotection may be related to the maintenance of Na^+, K^+-ATPase activity. [