Establishment of a local cooling model against spinal cord ischemia representing prolonged induction of heat shock protein.
Establishment of a local cooling model against spinal cord ischemia representing prolonged induction of heat shock protein.
复制标题
建立针对脊髓缺血的局部冷却模型，代表热休克蛋白的长时间诱导。
DOI：
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复制
发表时间：
2001
影响因子：
6
通讯作者：
K. Tabayashi
中科院分区：
文献类型：
--
作者：
N. Motoyoshi;M. Sakurai;Takeshi Hayashi;Masashi Aoki;Koji Abe;Y. Itoyama;K. Tabayashi
目标
截瘫是胸腹主动脉手术的严重并发症之一。局部低温对脊髓缺血有保护作用，但其保护机制尚不清楚。我们试图建立一个简单的模型，局部冷却下短暂的脊髓缺血和评估的影响，使用功能和组织学的结果。
方法
将雄性家兔分为对照组、常温组（N组）和局部低温组（H组）。通过腹主动脉夹闭，使用球囊导管治疗脊髓缺血。一个冰袋连接到腰部区域可以降低区域脊髓温度最初。采用约翰逊评分评价神经功能。采用苏木精-伊红染色、末端脱氧核苷酸转移酶介导的脱氧尿嘧啶三磷酸生物素原位缺口末端标记法（TUNEL）和热休克蛋白免疫反应性观察运动神经元的损伤情况。
结果
生理评估显示局部低温改善了功能缺陷（N组，1.3 +/- 0.9; H组，4.9 +/- 0.3; P = 0.0020）。再灌注7天后，N组和H组之间的运动神经元数量存在显著差异（N组，7.2 +/- 1.9; H组，20.4 +/- 3.2; P = 0.0090）。TUNEL阳性运动神经元的数量显著减少（N组，7.2 +/- 2.4; H组，1.0 +/- 0.7; P = 0.0082）。低温组热休克蛋白免疫反应延长至再灌注后2天。
结论
结果表明，局部低温延长了再灌注后脊髓运动神经元热休克蛋白的产生，抑制了其凋亡变化。
OBJECTIVES
Paraplegia is one of the serious complications of thoracoabdominal aortic operations. Regional hypothermia protects against spinal cord ischemia although the protective mechanism remains unknown. We attempted to create a simple model of local cooling under transient spinal cord ischemia and evaluated the effect using functional and histologic findings.
METHODS
Male domesticated rabbits were divided into 3 groups: control, normothermic group (group N), and local hypothermic group (group H). A balloon catheter was used for spinal cord ischemia by abdominal aortic clamping. A cold pack attached to the lumbar region could lower the regional cord temperature initially. Neurologic function was evaluated by the Johnson score. Cell damage was analyzed by observing motor neurons with the use of hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated deoxy-uracil triphosphate biotin in situ nick end labeling (TUNEL), and immunoreactivity of heat shock protein.
RESULTS
Physiologic estimation showed that local hypothermia improved the functional deficits (group N, 1.3 +/- 0.9; group H, 4.9 +/- 0.3; P =.0020). Seven days after reperfusion, there was a significant difference in the motor neuron numbers between groups N and H (group N, 7.2 +/- 1.9; group H, 20.4 +/- 3.2; P =.0090). The number of TUNEL-positive motor neurons was reduced significantly (group N, 7.2 +/- 2.4; group H, 1.0 +/- 0.7; P =.0082). Heat shock protein immunoreactivity was prolonged up to 2 days after reperfusion in the hypothermic group.
CONCLUSIONS
These results suggest that local hypothermia extended the production of heat shock protein in spinal cord motor neurons after reperfusion and inhibited their apoptotic change.
影响因子：
8.3
作者：
BUSTO, R;GLOBUS, MY;GINSBERG, MD
通讯作者：
GINSBERG, MD