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Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock

OBJECTIVES: The anesthetic gas xenon is reported to preserve hemodynamic stability during general anesthesia. However, the effects of the gas during shock are unclear. The objective of this study was to evaluate the effect of Xe on hemodynamic stability and tissue perfusion in a canine model of hemo...

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Autores principales: Franceschi, Ruben C., Malbouisson, Luiz, Yoshinaga, Eduardo, Auler, José Otavio Costa, de Figueiredo (in memoriam), Luiz Francisco Poli, Carmona, Maria José C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3584269/
https://www.ncbi.nlm.nih.gov/pubmed/23525321
http://dx.doi.org/10.6061/clinics/2013(02)OA18
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author Franceschi, Ruben C.
Malbouisson, Luiz
Yoshinaga, Eduardo
Auler, José Otavio Costa
de Figueiredo (in memoriam), Luiz Francisco Poli
Carmona, Maria José C.
author_facet Franceschi, Ruben C.
Malbouisson, Luiz
Yoshinaga, Eduardo
Auler, José Otavio Costa
de Figueiredo (in memoriam), Luiz Francisco Poli
Carmona, Maria José C.
author_sort Franceschi, Ruben C.
collection PubMed
description OBJECTIVES: The anesthetic gas xenon is reported to preserve hemodynamic stability during general anesthesia. However, the effects of the gas during shock are unclear. The objective of this study was to evaluate the effect of Xe on hemodynamic stability and tissue perfusion in a canine model of hemorrhagic shock. METHOD: Twenty-six dogs, mechanically ventilated with a fraction of inspired oxygen of 21% and anesthetized with etomidate and vecuronium, were randomized into Xenon (Xe; n = 13) or Control (C; n = 13) groups. Following hemodynamic monitoring, a pressure-driven shock was induced to reach an arterial pressure of 40 mmHg. Hemodynamic data and blood samples were collected prior to bleeding, immediately after bleeding and 5, 20 and 40 minutes following shock. The Xe group was treated with 79% Xe diluted in ambient air, inhaled for 20 minutes after shock. RESULT: The mean bleeding volume was 44 mL.kg(−1) in the C group and 40 mL.kg(−1) in the Xe group. Hemorrhage promoted a decrease in both the cardiac index (p<0.001) and mean arterial pressure (p<0.001). These changes were associated with an increase in lactate levels and worsening of oxygen transport variables in both groups (p<0.05). Inhalation of xenon did not cause further worsening of hemodynamics or tissue perfusion markers. CONCLUSIONS: Xenon did not alter hemodynamic stability or tissue perfusion in an experimentally controlled hemorrhagic shock model. However, further studies are necessary to validate this drug in other contexts.
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spelling pubmed-35842692013-03-01 Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock Franceschi, Ruben C. Malbouisson, Luiz Yoshinaga, Eduardo Auler, José Otavio Costa de Figueiredo (in memoriam), Luiz Francisco Poli Carmona, Maria José C. Clinics (Sao Paulo) Basic Research OBJECTIVES: The anesthetic gas xenon is reported to preserve hemodynamic stability during general anesthesia. However, the effects of the gas during shock are unclear. The objective of this study was to evaluate the effect of Xe on hemodynamic stability and tissue perfusion in a canine model of hemorrhagic shock. METHOD: Twenty-six dogs, mechanically ventilated with a fraction of inspired oxygen of 21% and anesthetized with etomidate and vecuronium, were randomized into Xenon (Xe; n = 13) or Control (C; n = 13) groups. Following hemodynamic monitoring, a pressure-driven shock was induced to reach an arterial pressure of 40 mmHg. Hemodynamic data and blood samples were collected prior to bleeding, immediately after bleeding and 5, 20 and 40 minutes following shock. The Xe group was treated with 79% Xe diluted in ambient air, inhaled for 20 minutes after shock. RESULT: The mean bleeding volume was 44 mL.kg(−1) in the C group and 40 mL.kg(−1) in the Xe group. Hemorrhage promoted a decrease in both the cardiac index (p<0.001) and mean arterial pressure (p<0.001). These changes were associated with an increase in lactate levels and worsening of oxygen transport variables in both groups (p<0.05). Inhalation of xenon did not cause further worsening of hemodynamics or tissue perfusion markers. CONCLUSIONS: Xenon did not alter hemodynamic stability or tissue perfusion in an experimentally controlled hemorrhagic shock model. However, further studies are necessary to validate this drug in other contexts. Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo 2013-02 /pmc/articles/PMC3584269/ /pubmed/23525321 http://dx.doi.org/10.6061/clinics/2013(02)OA18 Text en Copyright © 2013 Hospital das Clínicas da FMUSP http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Basic Research
Franceschi, Ruben C.
Malbouisson, Luiz
Yoshinaga, Eduardo
Auler, José Otavio Costa
de Figueiredo (in memoriam), Luiz Francisco Poli
Carmona, Maria José C.
Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title_full Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title_fullStr Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title_full_unstemmed Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title_short Evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
title_sort evaluation of hemodynamic effects of xenon in dogs undergoing hemorrhagic shock
topic Basic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3584269/
https://www.ncbi.nlm.nih.gov/pubmed/23525321
http://dx.doi.org/10.6061/clinics/2013(02)OA18
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