Diaphragm EMG activity during hyperbaric oxygen exposure in spinal injured rats

Abstract

Cervical spinal cord injury can cause significant respiratory dysfunction and in severe cases necessitates mechanical ventilation. Accumulating evidence indicates that hyperbaric oxygen (HBO) therapy, initiated shortly after spinal cord injury (SCI), can mitigate spinal cord pathology. Further, a recent study from our group demonstrated that HBO therapy can attenuate diaphragm atrophy after SCI. The primary purpose of the present investigation was to evaluate diaphragm electromyogram (EMG) activity during HBO therapy in rats with cervical SCI. HBO therapy has not been widely adopted after SCI, and if HBO is to be translated to human use, we reasoned that it is important to determine how breathing is impacted during HBO exposure. Adult female Sprague‐Dawley rats were implanted with chronic indwelling EMG electrodes in the mid‐costal diaphragm two weeks prior to SCI. Following hemicontusion injury of the C4 spinal cord, one experimental group was treated with HBO (n=3), and another group was left untreated (n=3). The HBO treatment consisted of a one hour exposure to 100% O2 at 3 atmospheres (ATA). In all experiments, diaphragm EMG activity was recorded in freely moving rats, without anesthesia. Recordings were made for 10 minutes prior to treatment, throughout the HBO exposure, and for 10 minutes after. Diaphragm EMG recordings in the normobaric normoxia control group conditions were completed for the same duration of time as the treated group. Daily HBO treatment and EMG recordings were done until 10‐days post‐SCI. Peak diaphragm EMG burst amplitude was quantified before SCI, over the 10 days of treatment, and at 1 and 2 weeks post‐treatment. Prior to SCI, body weight was similar between groups (control: 227±4 g; HBO: 228±3 g). All rats with tolerated HBO treatment with no evidence of adverse events or impact on weight gain over the 10 day period (10 day body weight: control: 198 ± 14 g; HBO: 197 ± 13 g). The acute HBO exposure caused an increase in the area under the curve of the rectified and integrated inspiratory burst amplitude of the diaphragm recording made ipsilateral to the lesion. This increase averaged 126 ± 18% of baseline across the 10 HBO treatments. The ipsilateral EMG burst amplitude also remained elevated at 10 min post‐HBO exposure (115 ± 32%) compared to pre HBO exposure. At the conclusion of the 10 day treatment paradigm, ipsilateral diaphragm EMG output during quiet breathing was elevated in HBO (156 ± 50% of post‐injury baseline) as compared to the control group (111 ± 6% of baseline). However the ipsilateral diaphragm EMG burst amplitude of the two groups were similar when evaluated 2 weeks after the daily HBO sessions concluded. This ongoing study indicates that acute exposure to HBO therapy is associated with an increase in diaphragm EMG activity, and 10 days of HBO therapy accelerates the recovery of diaphragm activation following cervical contusion injury.