A Mouse Model of Ischemic Spinal Cord Injury with Delayed Paralysis Caused by Aortic Cross-clamping

被引:51
作者
Awad, Hamdy [1 ]
Ankeny, Daniel P. [1 ]
Guan, Zhen [1 ]
Wei, Ping [1 ]
McTigue, Dana M. [1 ]
Popovich, Phillip G. [1 ]
机构
[1] Ohio State Univ, Coll Med, Dept Neurosci, Ctr Brain & Spinal Cord Repair, Columbus, OH 43210 USA
关键词
THORACOABDOMINAL ANEURYSM REPAIR; STATUS EPILEPTICUS; PARAPLEGIA; HYPOTHERMIA; OPERATIONS; KETAMINE; SURGERY; REPERFUSION; PROTECTION; BRAIN;
D O I
10.1097/ALN.0b013e3181ec61ee
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Spinal cord ischemia and paralysis are devastating perioperative complications that can accompany open or endovascular repair surgery for aortic aneurysms. Here, we report on the development of a new mouse model of spinal cord ischemia with delayed paralysis induced by cross-clamping the descending aorta. Methods: Transient aortic occlusion was produced in mice by cross-clamping the descending aorta through a lateral thoracotomy. To establish an optimal surgical procedure with limited mortality, variable cross-clamp times and core temperatures were tested between experiments. Results: The onset of paresis or paralysis and postsurgical mortality varied as a function of cross-clamp time and core temperature that was maintained during the period of cross-clamp. Using optimal surgical parameters (7.5-min cross-clamp duration at 33 degrees C core temperature), the onset of paralysis is delayed 24-36 h after reperfusion, and more than 95% of mice survive through 9 weeks after surgery. These mice are further stratified into two groups, 70% (n = 19/27) of mice developing severe hind limb paralysis and the remaining mice showing mild, though still permanent, behavioral deficits. Conclusion: This new model should prove useful as a preclinical tool for screening neuroprotective therapeutics and for defining the basic biologic mechanisms that cause delayed paralysis and neurodegeneration after transient spinal cord ischemia.
引用
收藏
页码:880 / 891
页数:12
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