Bronchopulmonary C fibers are the primary chemosensitive afferents in the lung. The activation of bronchopulmonary C fibers evokes the pulmonary chemoreflex, which is characterized by apnea, hypotension, and bradycardia and is a critical reflex that modulates cardiorespiratory responses under physiological and pathological conditions. The present study was designed to investigate whether the pulmonary chemoreflex is altered following acute cervical spinal injury. A unilateral hemisection (Hx) or laminectomy (uninjured) in the second cervical spinal cord was performed in adult male Sprague-Dawley rats. The pulmonary chemoreflex induced by intrajugular capsaicin administration was evaluated by measuring respiratory airflow in spontaneously breathing rats and phrenic nerve activity in mechanically ventilated rats. Capsaicin treatment evoked a cessation of respiratory airflow and phrenic bursting in uninjured animals, but not in C2Hx animals. To clarify whether the attenuation of the pulmonary chemoreflex in C2Hx animals is restricted to capsaicin-induced stimuli, or generally applied to other stimuli that excite bronchopulmonary C fibers, another bronchopulmonary C-fiber stimulant (phenylbiguanide) was used to evoke the pulmonary chemoreflex in spontaneously breathing rats. We observed that phenylbiguanide-induced apnea was also blunted in C2Hx animals, suggesting that the respiratory response induced by bronchopulmonary C-fiber activation was attenuated following acute cervical spinal Hx. The blunted inhibitory respiratory response may represent a compensatory respiratory plasticity to preserve the breathing capacity and may also reduce the capability of preventing inhaled irritants in this injured condition.
Keywords: bronchopulmonary C fiber; cervical spinal cord injury; phrenic; pulmonary chemoreflex.