Hyperbaric Oxygen Therapy Alters Vascular Reactivity Independent of Elevations in ATP

Abstract

Hyperbaric oxygen (HBO) is a pharmacologic therapy used treat a variety of medical conditions.  The underlying mechanisms of HBOs effect on vascular reactivity are poorly understood. The purpose of this study was to record the acute effects of HBO on vascular reactivity and determine the potential role of ATP in mediating these effects.  Porcine mesenteric arteries were dissected and mounted in isolated organ baths to record changes in tension in response to potassium chloride (KCl, 15-60 mM), phenylephrine (PHE, 10^-7-10^-4 M), and sodium nitroprusside (SNP, 10^-7-10^-4 M) following a 2-hour exposure to HBO (1.75 ATA).  HBO augmented responses to KCl and PHE compared to control arteries exposed to room air or nitrogen at 1.75 ATA as well as to room air at 1 atm. When compared to the 1 ATA room air control, KCl-induced constriction was significantly increased for the HBO exposure.  Treatment with HBO also augmented vascular responses to PHE and SNP relative to nitrogen, but not ambient air. We hypothesized that HBO increased ATP production in vascular smooth muscle leading to enhanced vascular reactivity.  Consequently, ATP levels were measured in mesenteric arteries but no significant differences in ATP levels were observed regardless of hyperbaric treatment.  Direct measurements of ATPs’ effects on porcine vasculature with and without hyperbaric treatment resulted in no significant findings. These results suggest that HBO alters vascular reactivity independent of elevations in ATP.