Evaluation of Hyperbaric Oxygen Therapy in the Treatment of Spinal Cord Injury Using the Rabbit Spinal Stroke Model.

摘要

This study examined the role of oxygen in the development of neuromotor dysfunction generated by temporary aortic occlusion in awake and anesthetized rabbit models of experimental spinal cord ischemia. Animals underwent 30 minutes of infrarenal aortic occlusion, via a pre-implanted aortic snare, followed by 15 minutes of reperfusion prior to treatment with one of three inhaled gas compositions: air (control), 100% oxygen (sea level oxygen), and 100% oxygen at 2.8 atmospheres pressure (hyperbaric oxygen). After the 90 minute treatment and at specific times thereafter, the animals hindlimb motor function was graded on a five point neuromotor index (4 = normal, 0 = total paralysis). Control animals were paralyzed after reperfusion but regained hindlimb neuromotor function within six hours after reperfusion and retained substantial hindlimb movement at 24 hours. However, both the sea level oxygen and hyperbaric oxygen groups failed to regain hindlimb neuromotor function within six hour and were totally paralyzed at 24 hours. Histopathological examination of the animals' spinal cord revealed good correlation between spinal cord damage and the clinical neurological outcome. In an alternative anesthetized model, hyperbaric oxygen treatment appeared to temporarily retard the post reperfusion improvement in neuromotor function. This phenomenon was not accompanied by an increase in tissue lipid peroxidation but was accompanied by post treatment hyperemia of the affected spinal cord segments. These data support the notion that the degree of inspired oxygen tension in the immediate reperfusion period may play a role in the development of spinal cord reperfusion injury.