Baroreflex-mediated cardiovascular responses to hyperbaric oxygen

Abstract

The cardiovascular system responds to hyperbaric hyperoxia (HBO₂) with vasoconstriction, hypertension, bradycardia, and reduced cardiac output (CO). We tested the hypothesis that these responses are linked by a common mechanism—activation of the arterial baroreflex. Baroreflex function in HBO₂ was assessed in anesthetized and conscious rats after deafferentation of aortic or carotid baroreceptors or both. Cardiovascular and autonomic responses to HBO₂ in these animals were compared with those in intact animals at 2.5 ATA for conscious rats and at 3 ATA for anesthetized rats. During O₂ compression, hypertension was greater after aortic or carotid baroreceptor deafferentation and was significantly more severe if these procedures were combined. Similarly, the hyperoxic bradycardia observed in intact animals was diminished after aortic or carotid baroreceptor deafferentation and replaced by a slight tachycardia after complete baroreceptor deafferentation. We found that hypertension, bradycardia, and reduced CO—the initial cardiovascular responses to moderate levels of HBO₂—are coordinated through a baroreflex-mediated mechanism initiated by HBO₂-induced vasoconstriction. Furthermore, we have shown that baroreceptor activation in HBO₂ inhibits sympathetic outflow and can partially reverse an O₂-dependent increase in arterial pressure.