Influence of decompression sickness on vasocontraction of isolated rat vessels

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 vasodi...

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Main Authors: Mazur, A., Lambrechts, K., Wang, Q., Belhomme, M., Theron, M., Buzzacott, Peter, Guerrero, F.
Format: Journal Article
Published: 2016
Online Access:http://hdl.handle.net/20.500.11937/71365
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author Mazur, A.
Lambrechts, K.
Wang, Q.
Belhomme, M.
Theron, M.
Buzzacott, Peter
Guerrero, F.
author_facet Mazur, A.
Lambrechts, K.
Wang, Q.
Belhomme, M.
Theron, M.
Buzzacott, Peter
Guerrero, F.
author_sort Mazur, A.
building Curtin Institutional Repository
collection Online Access
description 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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spelling curtin-20.500.11937-713652018-12-13T09:35:02Z Influence of decompression sickness on vasocontraction of isolated rat vessels Mazur, A. Lambrechts, K. Wang, Q. Belhomme, M. Theron, M. Buzzacott, Peter Guerrero, F. 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. 2016 Journal Article http://hdl.handle.net/20.500.11937/71365 10.1152/japplphysiol.00139.2015 restricted
spellingShingle Mazur, A.
Lambrechts, K.
Wang, Q.
Belhomme, M.
Theron, M.
Buzzacott, Peter
Guerrero, F.
Influence of decompression sickness on vasocontraction of isolated rat vessels
title Influence of decompression sickness on vasocontraction of isolated rat vessels
title_full Influence of decompression sickness on vasocontraction of isolated rat vessels
title_fullStr Influence of decompression sickness on vasocontraction of isolated rat vessels
title_full_unstemmed Influence of decompression sickness on vasocontraction of isolated rat vessels
title_short Influence of decompression sickness on vasocontraction of isolated rat vessels
title_sort influence of decompression sickness on vasocontraction of isolated rat vessels
url http://hdl.handle.net/20.500.11937/71365