1. Complex I syndrome in myocardial stunning and the effect of adenosine
- Author
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Laura B. Valdez, Alberto Boveris, Martín Donato, Darío E. Iglesias, Ricardo J. Gelpi, Silvina Sonia Bombicino, Verónica D'Annunzio, Bruno Buchholz, and Tamara Zaobornyj
- Subjects
Adenosine ,Mitochondrion ,Protein oxidation ,Biochemistry ,Mitochondria, Heart ,MYOCARDIAL ISCHEMIA/REPERFUSION ,chemistry.chemical_compound ,MITOCHONDRIA ,FREE RADICALS ,Heart metabolism ,Myocardial Stunning ,biology ,ADENOSINE ,PEROXYNITRITE ,Nitric oxide synthase ,Mitochondrial matrix ,Reperfusion Injury ,Rabbits ,COMPLEX I ,NITRIC OXIDE ,CIENCIAS NATURALES Y EXACTAS ,MYOCARDIAL STUNNING ,medicine.drug ,NITROTYROSINE ,medicine.medical_specialty ,Otras Ciencias Biológicas ,Heart Ventricles ,Cell Respiration ,TBARS ,Nitric oxide ,MTNOS ,Ciencias Biológicas ,Oxygen Consumption ,Physiology (medical) ,Internal medicine ,medicine ,MN-SOD ,Animals ,Myocardial stunning ,Electron Transport Complex I ,Superoxide Dismutase ,PROTEIN CARBONYLS ,medicine.disease ,Disease Models, Animal ,Endocrinology ,chemistry ,biology.protein ,Lipid Peroxidation ,Nitric Oxide Synthase - Abstract
Isolated rabbit hearts were exposed to ischemia (I; 15 min) and reperfusion (R; 5-30 min) in a model of stunned myocardium. I/R decreased left-ventricle O 2 consumption (46%) and malate-glutamate-supported mitochondrial state 3 respiration (32%). Activity of complex I was 28% lower after I/R. The pattern observed for the decline in complex I activity was also observed for the reduction in mitochondrial nitric oxide synthase (mtNOS) biochemical (28%) and functional (50%) activities, in accordance with the reported physical and functional interactions between complex I and mtNOS. Malate-glutamate-supported state 4 H 2O 2 production was increased by 78% after I/R. Rabbit heart Mn-SOD concentration in the mitochondrial matrix (7.4 ± 0.7 μM) was not modified by I/R. Mitochondrial phospholipid oxidation products were increased by 42%, whereas protein oxidation was only slightly increased. I/R produced a marked (70%) enhancement in tyrosine nitration of the mitochondrial proteins. Adenosine attenuated postischemic ventricular dysfunction and protected the heart from the declines in O 2 consumption and in complex I and mtNOS activities and from the enhancement of mitochondrial phospholipid oxidation. Rabbit myocardial stunning is associated with a condition of dysfunctional mitochondria named "complex I syndrome." The beneficial effect of adenosine could be attributed to a better regulation of intracellular cardiomyocyte Ca 2+ concentration. © 2011 Elsevier Inc. Fil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Zaobornyj, Tamara. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Bombicino, Silvina Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Iglesias, Dario Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Donato, Pablo Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: D'Anunzio, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: Buchholz, Bruno. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina
- Published
- 2011