The effects of cervical spinal cord injury on the pattern of breathing in the rat

Abstract

The principle cause of mortality and chronic morbidity after spinal cord injury (SCI) is respiratory failure. Hemisection of the second cervical spinal segment (C2HS) is frequently used as a model of SCI. The effects of this injury on breathing pattern, however, have not been investigated. The pattern of breathing was examined at 1-month (controls, n = 12; C2HS, n = 7) and 2-months postinjury (controls, n = 11; C2HS, n = 5). Measurements were made before and after bilateral vagotomy to determine the role of vagal afferents in the effects of injury. Rats were anesthetized with urethane and allowed to breathe room air spontaneously. Direct arterial blood pressure was measured with a calibrated pressure transducer from a catheter in the femoral artery positioned via cut down. Arterial blood gases were measured using an i-STAT analyzer. Normothermia was maintained throughout the study. A linear pneumotachometer was calibrated by standard methods before and after each study day and attached to the end of a tracheotomy tube and 30 minutes was allowed before measurements were taken. The inspiratory and expiratory airflow was measured before and after bilateral vagotomy. The airflow signal from the pneumotachometer was integrated to give expired tidal volume (VT). Respiratory rate (RR) was measured from the airflow signal. All data are presented as mean ± SD. Means for expired tidal volume were compared between animal groups using the Kruskal–Wallis anova and the Mann–Whitney U-test. All other means were compared using a two factor anova. Multiple comparisons were made using t-tests with Bonferroni's correction. No differences in blood pressure or blood gases were detected between groups. Injured rats maintained the same minute ventilation as controls by utilizing higher RR (minute−1) (1-month; controls 127 ± 19, injured 177 ± 31: 2-months; controls 126 ± 20, injured 168 ± 23) and lower VT (mL kg−1) (1-month; controls 8.6 ± 0.8, injured 6.9 ± 0.2: 2-months; controls 8.3 ± 0.7, injured 5.9 ± 0.2). In addition, the frequency of augmented breaths was greater in injured rats at 2-months postinjury compared to the 2-month control group (minute−1) (controls 0.12 ± 16, injured 0.45 ± 0.20). After bilateral vagotomy, VT increased and RR decreased in all groups and the pattern of breathing was no longer different between injured and control animals. In conclusion, the C2HS alters the pattern of breathing at 1- and 2-months postinjury and increases the frequency of augmented breaths at 2-months postinjury. These results also suggest that the pattern of breathing may be determined by the vagal mechanisms rather than impaired respiratory motor drive.