Influence of decompression sickness on vasocontraction of isolated rat vessels.
Studies conducted in divers indicate that endothelium function is impaired following a dive even without decompression sickness (DCS) Our previous experiment conducted on rat isolated vessels showed no differences in endothelium dependent vasodilation after a simulated dive even in the presence of DCS, while contractile response to phenylephrine was progressively impaired with increased decompression stress. This study aimed to further investigate the effect of DCS on vascular smooth muscle. Thirty two male Sprague Dawley rats were submitted to the same hyperbaric protocol and classified according to the severity of DCS: no DCS (without clinical symptoms) mild DCS, or severe DCS (dead within 1 h) A control group remained at atmospheric pressure. Isometric tension was measured in rings of abdominal aorta and mesenteric arteries. Single dose contraction was assessed with KCl solution. Dose response curves were obtained with phenylephrine and endothelin 1. Phenylephrine induced contraction was observed in the presence of antioxidant tempol. Additionally, plasma concentrations of angiotensin II, angiotensin converting enzyme, and thiobarbituric acid reactive substances (TBARS) were assessed. Response to phenylephrine was impaired only among mild DCS in both vessels. Dose response curves to endothelin 1 were impaired after mild DCS in mesenteric and severe DCS in aorta. KCl induced contraction was affected after hyperbaric exposure regardless of DCS status in aorta only. These results confirm postdive vascular dysfunction is dependent on the type of vessel. It further evidenced that vascular dysfunction is triggered by DCS rather than by diving itself and suggest the influence of circulating factor/s. Diving induced impairment of the L type voltage dependent Ca(2+ channels and/or influence of renin angiotensin system is proposed.
Journal of applied physiology