Cervical spinal cord injury typically results in respiratory impairments. Clinical and animal studies have demonstrated that respiratory function can spontaneously and partially recover over time after injury. However, it remains unclear whether respiratory recovery is associated with alterations in metabolism. The present study was designed to comprehensively examine ventilation and metabolism in a rat model of spinal cord injury. Adult male rats received sham (i.e., laminectomy) or unilateral mid-cervical contusion injury (height of impact rod: 6.25 or 12.5 mm). Breathing patterns and whole-body metabolism (O2 consumption and CO2 production) were measured using a whole-body plethysmography system conjugated with flow controllers and gas analyzer at the acute (1 day post-injury), subchronic (2 weeks post-injury), and chronic (8 weeks post-injury) injury stages. The results demonstrated that mid-cervical contusion caused a significant reduction in the tidal volume. Although the tidal volume of contused animals can gradually recover, it remains lower than that of uninjured animals at the chronic injury stage. While O2 consumption and CO2 production were similar between uninjured and contused animals at the acute injury stage, these two metabolic parameters were significantly reduced in contused animals at the subchronic to chronic injury stages. Additionally, the relationships between ventilation, metabolism, and body temperature were altered by cervical spinal cord injury. These results suggest that cervical spinal cord injury causes a complicated reconfiguration of ventilation and metabolism that may enable injured animals to maintain a suitable homeostasis for adapting to the pathophysiological consequences of injury.
Postinjury administration of 17β-estradiol induces protection in the gray and white matter with associated functional recovery after cervical spinal cord injury in male rats
