Unilateral high cervical spinal hemisection (i.e., C2Hx) interrupts the respiratory bulbospinal pathway and results in paralysis of the hemidiaphragm. The ipsilateral diaphragmatic activity can partially recover over weeks to months; however, its contribution to the tidal volume generation is less than 20%. Accordingly, we hypothesized that the contralateral diaphragm exerts a compensatory function to maintain the essential ventilation following C2Hx. The cardiorespiratory pattern and bilateral diaphragm electromyogram (EMG) signals were measured in urethane-anesthetized and spontaneously breathing adult rats at 1 day, and 2 or 8 weeks post-C2Hx or C2 laminectomy. The functional contribution of the diaphragm was assessed by measuring immediate changes of the tidal volume following phrenic nerve section. At 1 day post-injury, the tidal volume was significantly reduced after contralateral phrenicotomy in C2Hx animals (54 ± 3% decline) compared with uninjured controls (20 ± 2% decline). Moreover, the arterial carbon dioxide partial pressure was significantly elevated in C2Hx animals (from 76 ± 8 mmHg to 117 ± 5 mmHg) but not in uninjured animals (from 51 ± 4 mmHg to 55 ± 3 mmHg). By 2 and 8 weeks post-injury, contralateral phrenicotomy still caused a greater reduction in the tidal volume in C2Hx than in uninjured animals, and the percentage decline of the tidal volume was similar to the response at 1 day post-injury. These data suggested that unilateral cervical spinal cord injury induced a persistent compensatory plasticity in the contralateral diaphragm, which plays a critical role in maintenance of essential ventilation.
Keywords: cervical spinal cord injury; compensation; diaphragm; respiration.