Optimizing Hemodynamic Support of Acute Spinal Cord Injury Based on Injury Mechanism.

摘要

Our preliminary data of Year 1 sheds light on the dynamic changes that occur with oxygenation, blood flow, and metabolic responses in the penumbra of the traumatic spinal cord injury site. Spinal cord contusion followed by compression resulted in a prompt loss of perfusion at the sites nearest to the epicentre with a critical reduction of substrate (glucose/oxygen) delivery. Following decompression only partially recovery was observed for blood flow, oxygen and glucose and persisted for several hours. Distal to the injury we also observed a decrease in spinal cord oxygenation although more progressive over time, causing a continual increase in L/P ratio above baseline, suggesting that our experimental SCI caused widespread and sustained hypoxia. Although blood flow levels gradually recovered to baseline levels, however, failed to improve spinal cord oxygenation in our setting. In fact, tissue oxygenation was found to be entirely unaffected, reflected by an elevation in the L/P ratio. This data advances our current understanding of the pathophysiology following spinal cord injury, and in Year 2 we will focus of this study is to evaluate the consequences of hemodynamic support on intraparenchymal blood flow, oxygenation and downstream metabolic responses, after SCI.