Impact of Acute Hyperbaric Oxygen Treatment on Phrenic Motor Output in Adult Male Rats

Abstract

Hyperbaric oxygen (HBO) therapy involves exposure to 100% oxygen delivered above one atmosphere absolute (ATA), typically for ≤1 hour. HBO therapy is commonly used for promoting wound healing and treating decompression sickness. HBO treatment radically increases arterial oxygen content and can stimulate production of anti‐oxidants and suppress inflammation. These and other HBO‐induced responses could potentially impact the neural regulation of breathing. Here we investigated if exposure to HBO (100% O2, 2 ATA, 1 hr) impacts baseline phrenic motor output or the ability to express phrenic long term facilitation induced by acute intermittent hypoxia (AIH). Adult male Sprague‐Dawley rats were treated with HBO (n=8) or sham treatment (n=7, room air, 1 ATA), and then immediately urethane‐anesthetized and mechanically ventilated. Rats were vagotomized and phrenic nerve output was recorded using a suction electrode. On average, 86±23 min elapsed from the end to HBO treatment to the initiation of phrenic recordings. After establishing the CO2 apneic and recruitment thresholds, a stable baseline was maintained at 2 mmHg above of recruitment threshold for 15‐20 min. Rats were then exposed to AIH which consisted of three 5‐min episodes of moderate hypoxia (arterial partial pressure of O2, PaO2, approximately 45 mmHg) separated by 5‐min intervals of baseline O2conditions. Arterial samples were drawn at baseline, during hypoxia and every 20 min following AIH for blood‐gas analysis. Phrenic activity was recorded for 60 min after AIH. An unpaired two‐tailed t‐test was applied to compare baseline (BL) parameters between groups. Analysis of long term facilitation of phrenic burst amplitude after AIH (expressed as %BL) was done using two‐way repeated measures ANOVA. The HBO treatment did not affect baseline parameters including phrenic burst amplitude (p=0.34), burst frequency (p=0.48), mean arterial blood pressure (p=0.66), PaO2 (p=0.86) or PaCO2 (p=0.27). Phrenic LTF tended to be greater in the HBO group (burst amplitude 81±50 %BL at 60 min) as compared to control (43±9 %BL at 60 min). However, this difference was not statistically significant (treatment effect, P=0.16). Our preliminary conclusion is that a single session of HBO at 2 ATA for 1 hour has no detectable impact on baseline phrenic motor output recorded approximately 90 minutes after end of the HBO treatment. Additional experiments are needed before drawing a firm conclusion regarding the impact of HBO on phrenic long‐term facilitation.