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Am J Physiol Heart Circ Physiol (January 24, 2002). doi:10.1152/ajpheart.00471.2001
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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00471.2001
Submitted on May 31, 2001
Accepted on September 19, 2001

ALTERATION OF MITOCHONDRIAL FUNCTION IN A MODELE OF CHRONIC ISCHEMIA IN VIVO IN RAT HEART

SIHEM BOUDINA1, MURIEL N LACLAU1, LILIANE TARIOSSE1, DANNIELE DARET1, GERARD GOUVERNEUR1, SIMONE BONORON-ADELE1, VALDUR A SAKS2, and PIERRE DOS SANTOS1*

1 Atherosclerosis, INSERM U441, Pessac, France, France
2 FourrierLaboratory of Bioenergetics, Universite Joseph, Grenoble, France, France; Laboratory of Bioenergetics, National Institute of Chemical and Biological Physics, Tallinn, Estonia, Estonia

The aim of this study is to investigate mitochondrial alterations in an animal model of chronic myocardial ischemia in rats obtained by surgical constriction of left coronary artery. Resting coronary blood flow was measured using the fluorescent microsphere technique. Contractile function, defined by rate pressure product, and myocardial oxygen consumption were measured in a Langendorff preparation. The mitochondrial function was evaluated on permeabilized skinned fibers. Three weeks after surgery, ischemic hearts showed a significant decrease in coronary blood flow compared to sham. Hemodynamic measurements showed a significant systolic and diastolic dysfunction. Alterations in mitochondrial function in ischemic hearts were mainly characterized by a significant decrease in Vmax and apparent K1/2 for ADP, loss of the stimulatory effect of creatine and a stimulatory effect of exogenous cytochrome c. These functional alterations were supported by structural alterations characterized by mitochondrial clustering and swelling associated with membrane rupture. We conclude that the alterations in systolic function after chronic ischemia are supported by severe modifications of mitochondrial structure and function.




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