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One half century has passed since the earliest reports of successful surgery on the thoracic aorta. While many of the early technical hurdles of thoracic aortic surgery are of historical interest only, spinal cord injury as a result of cord ischemia is still not routinely preventable. Irreversible spinal cord injury resulting in paraplegia or paraparesis is the single most devastating complication of surgery on the thoracic and thoracoabdominal aorta. Surgical series have documented permanent spinal cord dysfunction in 15 to 38% of high risk patients. Rarely, spinal cord injury rates are reported that are less than 5%. Although many technical and pharmacologic adjuncts have been described and tested to decrease the risk of spinal cord injury none have been so successful as to become standard of care. An aging population and a growing number of young trauma victims have contributed to an increasing number of operations for atherosclerotic and traumatic thoracic and thoracoabdominal aortic disease. A reliable and safe method of spinal cord protection is needed to offer these patients surgery without the risk of lifetime functional impairment.
The central theme of our research is to prevent spinal cord injury through the use of retrograde venous spinal cord perfusion. The theory of “retrograde perfusion” is similar to the delivery of retrograde cardioplegia to protect the heart from ischemic injury during cardiac surgery. Our technique of retrograde temperature-controlled venous perfusion allows us to investigate the efficacy of delivering cold (or warm) neuro-protective agents directly to the cord through retrograde venous perfusion, limiting the systemic effects of these agents (when compared to agents delivered peripherally). We also investigate mechanisms to cool the cord by retrograde perfusion and yet avoid systemic hypothermia.
Basic science model
We have developed reliable models of spinal cord ischemia and reperfusion in both rabbit and porcine animals. We use these models to further investigate the mechanisms of spinal cord ischemia and injury at the cellular level. Our model affords us the ability to induce an injury and study the effects histologically and functionally. Our technique of retrograde perfusion allows high concentrations of drugs to be delivered regionally, thereby avoiding systemic side effects. Previous studies have been limited in this fashion. Animals (and humans) cannot tolerate the systemic effects of many known neuro-protective agents. Delivering these agents directly to the cord in high doses has been difficult and impractical using standard intra-arterial, peripheral intra-venous, or intra-thecal techniques. Therefore, the full therapeutic potential of these agents in vivo has not been adequately assessed. Our models of cord injury and ischemia also allow us to directly correlate histologic findings to functional outcome. We begun to identify patterns of injury, such as cellular apoptosis, that may be uniquely different depending on the mode of injury. The effects of intervention on these patterns of injury are being determined and correlated to functional results.