Influence of decompression sickness on vasocontraction of isolated rat vessels

Abstract

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.

Time Course of Endothelial Dysfunction Induced by Decompression Bubbles in Rats

“…Vascular endothelial cells are well-described targets for decompression stress and endothelial injury plays an important role in the process of DCS (Lambrechts et al, 2013; Mazur et al, 2014, 2016; Fok et al, 2015; Wang et al, 2015), though the exact mechanism remains unclear. Whether bubbles are the cause or not, endothelial dysfunction is detectable and obvious following most diving exposures (Madden and Laden, 2009; Chrismas et al, 2010; Klinger et al, 2011; Papadopoulou et al, 2014).…”

Endothelial dysfunction correlates with decompression bubbles in rats

“…Because tiny moving microbubbles cannot be detected by current ultrasound techniques, the possibility remains that bubbles could have existed in the arterial system. In human divers, even large venous bubbles do cross to systemic arteries via right-to-left shunts including patent foramen ovale 20 and, although bubble detection was not performed, insults to arterial smooth muscle have been reported in a rat DCS model while endothelial function remained unchanged 31 32 .…”

Angiotensin Converting Enzyme Inhibitor Has a Protective Effect on Decompression Sickness in Rats

“…Because both age and weight are known to influence the probability of DCS (Buzzacott et al, 2016 ), animals used in these experiments were all the same age (12 weeks old) and similar weights (450 ± 50 g) on the day of the experiment. The simulated dive protocol has been previously described (Mazur et al, 2016 ). Briefly, rats from each group were placed in a dry hyperbaric chamber.…”

“…One possible, and repeatedly hypothesized, mechanism could rely on the well-documented diving-induced impairment of vascular function (Brubakk et al, 2005 ; Lambrechts et al, 2013a ; Mazur et al, 2016 ). In line with this hypothesis, administration of nitric oxide (NO) donors decreases both the amount of circulating bubbles (Dujić et al, 2006 ; Møllerløkken et al, 2006 ) and the probability of DCS (Wisløff et al, 2004 ), while blockade of NO production increases the probability of DCS (Wisloff et al, 2003 ; Mazur et al, 2014 ).…”

“…Indeed, altered vascular permeability (Gempp et al, 2013 ), platelet aggregation (Pontier et al, 2012 ), release of microparticles and inflammation (Thom et al, 2015 ), as well as oxidative stress (Mazur et al, 2016 ) have been evidenced post-dive. Recently, we found that plasmatic concentration of AngII was decreased after the dive in asymptomatic rats but not animals which suffered DCS (Mazur et al, 2016 ). This led us to hypothesize that maintaining the concentration of circulating Ang II could be part of the mechanisms leading to DCS.…”