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(Reference retrieved automatically from SciELO through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Cardioprotective effects of pharmacological blockade of the mitochondrial calcium uniporter on myocardial ischemia-reperfusion injury

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Author(s):
Francisco Sandro Menezes-Rodrigues [1] ; José Gustavo Padrão Tavares [2] ; Enio Rodrigues Vasques [3] ; Paolo Ruggero Errante [4] ; Erisvaldo Amarante de Araújo [5] ; Marcelo Pires-Oliveira [6] ; Carla Alessandra Scorza [7] ; Fúlvio Alexandre Scorza [8] ; Murched Omar Taha [9] ; Afonso Caricati-Neto [10]
Total Authors: 10
Affiliation:
[1] Universidade Federal de São Paulo. Postgraduate Program in Pharmacology - Brasil
[2] Universidade Federal de São Paulo. Postgraduate Program in Pharmacology - Brasil
[3] Universidade de São Paulo. School of Medicine. Laboratory of Liver Surgery and Transplant - Brasil
[4] UNIFESP. Postgraduate Program in Pharmacology - Brasil
[5] UNIFESP. Postgraduate Program in Pharmacology - Brasil
[6] União Metropolitana de Educação e Cultura. School of Medicine - Brasil
[7] UNIFESP. Department of Neurology and Neurosurgery - Brasil
[8] UNIFESP. Department of Neurology and Neurosurgery - Brasil
[9] UNIFESP. Department of Surgery - Brasil
[10] UNIFESP. Department of Pharmacology - Brasil
Total Affiliations: 10
Document type: Journal article
Source: Acta Cirurgica Brasileira; v. 35, n. 3 2020-05-20.
Abstract

Abstract Purpose To evaluate whether the attenuation of mitochondrial Ca2+ overload produced by pharmacological blockade of mitochondrial Ca2+ uniporter (MCU) protects the myocardium against injuries caused by cardiac ischemia and reperfusion (CIR). Methods CIR was induced in adult male Wistar rats (300-350 g) by occlusion of the left anterior descendent coronary artery (10 min), followed by reperfusion (120 min). Rats were treated with different doses of MCU blocker ruthenium red (RuR), administered 5 min before ischemia or reperfusion. Results In untreated rats, the incidences of ventricular arrhythmias (VA), atrioventricular block (AVB) and the lethality (LET) induced by CIR were 85%, 79% and 70%, respectively. In rats treated with RuR before ischemia, the incidences of VA, AVB and LET were significantly reduced to 62%, 25% and 25%, respectively. In rats treated with RuR after ischemia, the incidences of VA, AVB and LET were significantly reduced to 50%, 25% and 25%, respectively. Conclusion The significant reduction of the incidence of CIR-induced VA, AVB and LET produced by the treatment with RuR indicates that the attenuation of mitochondrial Ca2+ overload produced by pharmacological blockade of MCU can protect the myocardium against injuries caused by CIR. (AU)

FAPESP's process: 17/25565-1 - New therapeutic approach of the Parkinson´s disease: Neuroprotection stimulated by pharmacological modulation of the intracellular signaling by Ca2+/cAMP/NO
Grantee:Afonso Caricati Neto
Support Opportunities: Regular Research Grants