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Oxidative phosphorylation and respiration by mitochondria from normal, hypertrophied and failing rat hearts.
Authors:T J Raczniak  C F Chesney  J R Allen
Affiliation:1. Department of Pathology, University of Wisconsin Medical School, Madison, Wisconsin 53706, U.S.A.;2. Regional Primate Center, University of Wisconsin, Madison, Wisconsin 53706, U.S.A.
Abstract:The present study was undertaken in order to determine the differences in mitochondrial respiration and oxidative phosphorylation of the myocardium from rats with monocrotaline pyrrole induced pulmonary heart disease. Experimental animals developed right ventricular hypertrophy and heart failure 6 weeks post monocrotaline pyrrole injection. Respiratory function of heart mitochondria in glutamate and succinate substrates was evaluated polarographically. Mitochondrial electron transport and phosphorylating efficiency increased slightly during cardiac hypertrophy, began to decline during impending cardiac failure, and was markedly impaired in congestive heart failure.
Keywords:Oxidative phosphorylation  Cardiac hypertrophy  Mitochondria  Congestive heart failure  Rat heart  Monocrotaline pyrrole
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