Grant: Operating Grant

Each year, over 1,700 Canadians are paralyzed after suffering an acute traumatic spinal cord injury (SCI). Unfortunately, current treatment options for acute SCI are extremely limited. These include surgical decompression to relieve pressure on the cord, and support of systemic blood pressure to augment spinal cord blood flow. Current practice guidelines supported by weak clinical evidence recommend using intravenous fluids and vasopressors to maintain the mean arterial pressure (MAP) at 85-90 mm Hg for 5-7 days post-injury. By promoting a 'one-size-fits-all' approach, such hemodynamic guidelines ignore the possibility that the spinal cord and its blood flow respond differently depending upon whether the cord remains compressed or has been surgically decompressed after a period of prolonged compression lasting hours to days. The ultimate goal of our research is to inform clinical guidelines around the hemodynamic management of acute SCI patients by determining how alterations in systemic blood pressure influence the injured spinal cord before and after surgical decompression. Our overall objective is to determine how hemodynamic support of systemic blood pressure in the presence or absence of spinal cord compression affects the vascular, metabolic, biochemical, and behavioral outcomes of traumatic SCI. Using a large animal model of SCI, we hypothesize that well-intended increases in MAP will exacerbate a so-called 'reperfusion' injury and ultimately have deleterious effects on regions of the spinal cord surrounding the injury site. Ultimately, a better understanding of how the spinal cord adjacent to the injury site responds to alterations in systemic blood pressure in the presence or absence of residual mechanical compression will help clinicians provide optimal hemodynamic management for patients with acute SCI and improve their chances of neurologic recovery.