Acute hyperoxia improves spinal cord oxygenation and circulatory function following cervical spinal cord injury in the rat

Abstract

AbstractSpinal cord injury is associated with spinal vascular disruptions that result in spinal ischemia and tissue hypoxia. This study evaluated the therapeutic efficacy of normobaric hyperoxia on spinal cord oxygenation and circulatory function at the acute stage of cervical spinal cord injury. Adult male Sprague–Dawley rats underwent dorsal cervical laminectomy or cervical spinal cord contusion. At 1–2 days after spinal surgery, spinal cord oxygenation was monitored in anesthetized and spontaneously breathing rats via the optical recording of oxygen sensor foils placed on the cervical spinal cord and pulse oximetry. The arterial blood pressure, heart rate, blood gases, and peripheral oxyhemoglobin saturation were also measured under hyperoxic (50% O2) and normoxic (21% O2) breathing. The results showed that contused animals had a significantly lower spinal cord oxygenation level than uninjured animals during normoxia. Cervical spinal cord contusion also significantly reduced peripheral oxyhemoglobin saturation, arterial oxygen partial pressure, and mean arterial blood pressure. Notably, the spinal oxygenation of contused rats could be improved to a level comparable to uninjured animals under hyperoxia. Furthermore, acute hyperoxia could elevate blood pressure, arterial oxygen partial pressure, and peripheral oxyhemoglobin saturation. These results suggest that normobaric hyperoxia can significantly improve spinal cord oxygenation and circulatory function during acute cervical spinal cord injury. We propose that adjuvant normobaric hyperoxia combined with other hemodynamic optimization strategies may prevent secondary damage after spinal cord injury and improve functional recovery.