Development of a simplified spinal cord ischemia model in mice.

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Use of genetically manipulated mice facilitates understanding pathological mechanisms in many diseases and contributes to therapy development. However, there is no practical and clinically relevant mouse model available for spinal cord ischemia. This report introduces a simplified long-term outcome mouse model of spinal cord ischemia. Male C57Bl/6J mice were anesthetized with isoflurane and endotracheally intubated. The middle segment of the thoracic aorta was clamped for 0, 8, 10 or 12 min via left lateral thoracotomy. Rectal temperature was maintained at 37.0+/-0.5 degrees C. A laser Doppler probe was used to measure lumbar spinal cord blood flow during thoracic aorta cross-clamping. Open field locomotor function and rotarod performance were evaluated at 1h and 1, 3, 5, and 7 days post-injury. Surviving neurons in the lumbar ventral horn were counted at 7 days post-injury. Cross-clamping the middle segment of the thoracic aorta resulted in approximately 90% blood flow reduction in the lumbar spinal cord. Neurological deficit and neuronal cell death were associated with ischemia duration. Another set of mice were subjected to 10 min aortic clamping or sham surgery and neurological function was examined at 1h and 1, 3, 5, 7, 14, and 28 days. Four of 5 mice (80%) in the injured group survived 28 days and had significant neurological deficit. This study indicates that cross-clamping of the aorta via left thoracotomy is a simple and reliable method to induce spinal cord ischemia in mice allowing definition of long-term outcome.





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Wang, Z, W Yang, GW Britz, FW Lombard, DS Warner and H Sheng (2010). Development of a simplified spinal cord ischemia model in mice. Journal of neuroscience methods, 189(2). pp. 246–251. 10.1016/j.jneumeth.2010.04.003 Retrieved from

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Wei Yang

Professor in Anesthesiology

Huaxin Sheng

Associate Professor in Anesthesiology

We have successfully developed various rodent models of brain and spinal cord injuries in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma, subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression injury. We also established cardiac arrest and hemorrhagic shock models for studying multiple organ dysfunction.  Our current studies focus on two projects. One is to examine the efficacy of catalytic antioxidant in treating cerebral ischemia and the other is to examine the efficacy of post-conditioning on outcome of subarachnoid hemorrhage induced cognitive dysfunction.

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