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Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart
Lasalocid, a specific mobile membrane ionophore for calcium, dopamine and norepinephrine was assayed in its capacity to reduce or maintain unaltered the cardiovascular function in conditions of imminent myocardial injury. In experiments of coronary blockade and reperfusion carried out in rat heart,...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394521/ https://www.ncbi.nlm.nih.gov/pubmed/30191481 http://dx.doi.org/10.1007/s11010-018-3437-2 |
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author | Estrada-Orihuela, Sergio F. Ibarra-Pérez, Carlos |
author_facet | Estrada-Orihuela, Sergio F. Ibarra-Pérez, Carlos |
author_sort | Estrada-Orihuela, Sergio F. |
collection | PubMed |
description | Lasalocid, a specific mobile membrane ionophore for calcium, dopamine and norepinephrine was assayed in its capacity to reduce or maintain unaltered the cardiovascular function in conditions of imminent myocardial injury. In experiments of coronary blockade and reperfusion carried out in rat heart, it was found that when administered from 5 to 30 minutes prior to the induction of coronary blockade, at a concentration of 2 mg/kg of body weight, the ionophore immediately, simultaneously, and completely interrupts the blood pressure decay, cardiac frequency increase, electrical ventricular tachycardia and fibrillation, as well as the fall of mitochondrial oxidative phosphorylation and decay of mitochondrial oxygen uptake provoked by the induced myocardial injury. It appears that the molecular mode of action of the lasalocid is associated with its unique ability to transport both calcium and the catecholamines, dopamine and norepinephrine, across mitochondrial and bimolecular lipid membranes, as well as through synaptic cell membrane terminals from rat heart, myocardial fibers of the heart and heart chromaffin membrane vesicles. It is suggested that for the potential medical use of lasalocid to detain incoming ischemic myocardial damage, there exists a need to develop a personal electronic device able to simultaneously monitor, detect, and inform on the very early and simultaneous signs of cardiac alterations of electrical, mechano-chemical, metabolic and hydraulic nature, all which precede heart failure and to administer the lasalocid. |
format | Online Article Text |
id | pubmed-6394521 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-63945212019-03-15 Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart Estrada-Orihuela, Sergio F. Ibarra-Pérez, Carlos Mol Cell Biochem Article Lasalocid, a specific mobile membrane ionophore for calcium, dopamine and norepinephrine was assayed in its capacity to reduce or maintain unaltered the cardiovascular function in conditions of imminent myocardial injury. In experiments of coronary blockade and reperfusion carried out in rat heart, it was found that when administered from 5 to 30 minutes prior to the induction of coronary blockade, at a concentration of 2 mg/kg of body weight, the ionophore immediately, simultaneously, and completely interrupts the blood pressure decay, cardiac frequency increase, electrical ventricular tachycardia and fibrillation, as well as the fall of mitochondrial oxidative phosphorylation and decay of mitochondrial oxygen uptake provoked by the induced myocardial injury. It appears that the molecular mode of action of the lasalocid is associated with its unique ability to transport both calcium and the catecholamines, dopamine and norepinephrine, across mitochondrial and bimolecular lipid membranes, as well as through synaptic cell membrane terminals from rat heart, myocardial fibers of the heart and heart chromaffin membrane vesicles. It is suggested that for the potential medical use of lasalocid to detain incoming ischemic myocardial damage, there exists a need to develop a personal electronic device able to simultaneously monitor, detect, and inform on the very early and simultaneous signs of cardiac alterations of electrical, mechano-chemical, metabolic and hydraulic nature, all which precede heart failure and to administer the lasalocid. Springer US 2018-09-06 2019 /pmc/articles/PMC6394521/ /pubmed/30191481 http://dx.doi.org/10.1007/s11010-018-3437-2 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Article Estrada-Orihuela, Sergio F. Ibarra-Pérez, Carlos Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title | Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title_full | Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title_fullStr | Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title_full_unstemmed | Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title_short | Lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
title_sort | lasalocid immediately and completely prevents the myocardial damage caused by coronary ischemia reperfusion in rat heart |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394521/ https://www.ncbi.nlm.nih.gov/pubmed/30191481 http://dx.doi.org/10.1007/s11010-018-3437-2 |
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