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Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning
Anesthetics modify regional left ventricular (LV) dysfunction following ischemia/reperfusion but their effects on global function in this setting are less clear. Aim of this study was to test the hypothesis that xenon would limit global LV dysfunction as caused by acute anterior wall ischemia, compa...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110144/ https://www.ncbi.nlm.nih.gov/pubmed/27867480 http://dx.doi.org/10.4103/2045-9912.191358 |
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author | Baumert, Jan-H. Roehl, Anna B. Funcke, Sandra Hein, Marc |
author_facet | Baumert, Jan-H. Roehl, Anna B. Funcke, Sandra Hein, Marc |
author_sort | Baumert, Jan-H. |
collection | PubMed |
description | Anesthetics modify regional left ventricular (LV) dysfunction following ischemia/reperfusion but their effects on global function in this setting are less clear. Aim of this study was to test the hypothesis that xenon would limit global LV dysfunction as caused by acute anterior wall ischemia, comparable to ischemic preconditioning. In an open-chest model under thiopental anesthesia, 30 pigs underwent 60-minute left anterior descending coronary artery occlusion, followed by 120 minutes of reperfusion. A xenon group (constant inhalation from previous to ischemia through end of reperfusion) was compared to control and ischemic preconditioning. Load-independent measures of diastolic function (end-diastolic pressure-volume relation, time constant of relaxation) and systolic function (end-systolic pressure-volume relation, preload-recruitable stroke work) were determined. Heart rate, arterial pressure, cardiac output, and arterial elastance were recorded. Data were compared in 26 pigs. Ischemia impaired global diastolic but not systolic function in control, which recovered during reperfusion. Xenon limited and preconditioning abolished diastolic dysfunction during ischemia. Arterial pressure decreased during reperfusion while arterial elastance increased. Tachycardia and antero-septal wall edema during reperfusion were observed in all groups. In spite of ischemia of 40% of LV mass, global systolic function was preserved. Deterioration in global diastolic function was limited by xenon and prevented by preconditioning. |
format | Online Article Text |
id | pubmed-5110144 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-51101442016-11-18 Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning Baumert, Jan-H. Roehl, Anna B. Funcke, Sandra Hein, Marc Med Gas Res Original Article Anesthetics modify regional left ventricular (LV) dysfunction following ischemia/reperfusion but their effects on global function in this setting are less clear. Aim of this study was to test the hypothesis that xenon would limit global LV dysfunction as caused by acute anterior wall ischemia, comparable to ischemic preconditioning. In an open-chest model under thiopental anesthesia, 30 pigs underwent 60-minute left anterior descending coronary artery occlusion, followed by 120 minutes of reperfusion. A xenon group (constant inhalation from previous to ischemia through end of reperfusion) was compared to control and ischemic preconditioning. Load-independent measures of diastolic function (end-diastolic pressure-volume relation, time constant of relaxation) and systolic function (end-systolic pressure-volume relation, preload-recruitable stroke work) were determined. Heart rate, arterial pressure, cardiac output, and arterial elastance were recorded. Data were compared in 26 pigs. Ischemia impaired global diastolic but not systolic function in control, which recovered during reperfusion. Xenon limited and preconditioning abolished diastolic dysfunction during ischemia. Arterial pressure decreased during reperfusion while arterial elastance increased. Tachycardia and antero-septal wall edema during reperfusion were observed in all groups. In spite of ischemia of 40% of LV mass, global systolic function was preserved. Deterioration in global diastolic function was limited by xenon and prevented by preconditioning. Medknow Publications & Media Pvt Ltd 2016-10-14 /pmc/articles/PMC5110144/ /pubmed/27867480 http://dx.doi.org/10.4103/2045-9912.191358 Text en Copyright: © 2016 Medical Gas Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. |
spellingShingle | Original Article Baumert, Jan-H. Roehl, Anna B. Funcke, Sandra Hein, Marc Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title | Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title_full | Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title_fullStr | Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title_full_unstemmed | Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title_short | Xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
title_sort | xenon protects left ventricular diastolic function during acute ischemia, less than ischemic preconditioning |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5110144/ https://www.ncbi.nlm.nih.gov/pubmed/27867480 http://dx.doi.org/10.4103/2045-9912.191358 |
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