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    Influence of decompression sickness on vasocontraction of isolated rat vessels

    Access Status
    Fulltext not available
    Authors
    Mazur, A.
    Lambrechts, K.
    Wang, Q.
    Belhomme, M.
    Theron, M.
    Buzzacott, Peter
    Guerrero, F.
    Date
    2016
    Type
    Journal Article
    
    Metadata
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    Citation
    Mazur, A. and Lambrechts, K. and Wang, Q. and Belhomme, M. and Theron, M. and Buzzacott, P. and Guerrero, F. 2016. Influence of decompression sickness on vasocontraction of isolated rat vessels. Journal of applied physiology (Bethesda, Md. : 1985). 120 (7): pp. 784-791.
    Source Title
    Journal of applied physiology (Bethesda, Md. : 1985)
    DOI
    10.1152/japplphysiol.00139.2015
    ISSN
    8750-7587
    School
    School of Nursing, Midwifery and Paramedicine
    URI
    http://hdl.handle.net/20.500.11937/71365
    Collection
    • Curtin Research Publications
    Abstract

    Copyright © 2016 the American Physiological Society. 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. Doseresponse 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 Ca2+ channels and/or influence of reninangiotensin system is proposed.

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