Abstract
The present study was designed to investigate laryngeal function responses to chemoreceptor activation after unilateral high-cervical spinal cord contusion in rats. Adult male Sprague–Dawley rats received laminectomy or unilateral contusion at the C2 spinal cord. Both respiratory airflow and subglottal pressure were measured in spontaneously breathing rats at three days, two weeks, or six weeks after spinal surgery. Laryngeal closure responses were evoked via intrajugular capsaicin (1.5 μg/kg) administration and hypoxia (12.5% O2, 3 min) to activate bronchopulmonary C-fibers and chemoreceptors, respectively. High cervical contusion resulted in long-term reductions in tidal volume without changes in laryngeal resistance at baseline. Alternatively, capsaicin-induced increased subglottal pressure was significantly attenuated in contused rats at three days post-injury. Contused rats regained the ability to increase laryngeal resistance after capsaicin treatment at two and six weeks post-injury, whereas this recovered response remained weaker than uninjured animals. Notably, hypoxia-induced laryngeal closure was not altered during the acute injured stage, but instead was blunted at six weeks post-injury. These data suggest that cervical spinal cord injury not only influences the breathing pattern, but it also impacts upper airway function through modulation of laryngeal resistance. An attenuated laryngeal closure response may negatively impact the ability to prevent irritant inhalation and maintenance of the functional residual capacity. This may contribute to the provocation of pulmonary disease after cervical spinal cord injury.
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