title: Complex I syndrome in myocardial stunning and the effect of adenosine.
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(2)O(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.
authors: Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, C1113AAD Buenos Aires, Argentina. lbvaldez@ffyb.uba.ar
authors: Laura B
authors: LB
authors: Valdez
authors: Tamara
authors: T
authors: Zaobornyj
authors: Silvina
authors: S
authors: Bombicino
authors: Darío E
authors: DE
authors: Iglesias
authors: Alberto
authors: A
authors: Boveris
authors: Martin
authors: M
authors: Donato
authors: Verónica
authors: V
authors: D'Annunzio
authors: Bruno
authors: B
authors: Buchholz
authors: Ricardo J
authors: RJ
authors: Gelpi
mesh_terms: D000241:Adenosine / Q000008:administration & dosage*; D000818:Animals; D019069:Cell Respiration / Q000187:drug effects; D004195:Disease Models, Animal; D042967:Electron Transport Complex I / Q000378:metabolism*; D006352:Heart Ventricles / Q000473:pathology; D015227:Lipid Peroxidation; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D017682:Myocardial Stunning / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D011817:Rabbits; D015427:Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D042967:Electron Transport Complex I; D000241:Adenosine