Impact of cervical spinal cord injury on the relationship between the metabolism and ventilation in rats

• Published in: Journal of applied physiology (1985) Vol. 131; no. 6; pp. 1799 - 1814
• Main Authors: Chiu, Tzu-Ting, Lee, Kun-Ze
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.12.2021
• Subjects: Animals; Body temperature; Carbon dioxide; Cervical Cord; Contusions; Gas analyzers; Homeostasis; Injury prevention; Male; Mechanical ventilation; Metabolism; Oxygen consumption; Plethysmography; Rats; Rats, Sprague-Dawley; Reconfiguration; Recovery of Function; Respiration; Respiratory function; Rodents; Spinal Cord; Spinal Cord Injuries; Tidal Volume; Ventilation; cervical spinal cord injury; metabolism; respiration
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00472.2021

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 (O consumption and CO production) were measured using a whole body plethysmography system conjugated with flow controllers and gas analyzer at the acute (1 day postinjury), subchronic (2 wk postinjury), and chronic (8 wk postinjury) 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. Although O consumption and CO 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. Ventilation and metabolism are tightly coupled to maintain appropriate energy expenditure under physiological conditions. Our findings demonstrate that cervical spinal cord injury results in the differential reduction of ventilation and metabolism at the various injury stages and leads to alterations in the relationship between ventilation and metabolism. These results from an animal model provide fundamental knowledge for understanding how cervical spinal cord injury impacts energy homeostasis.