Why are ATP depletion rates in situ in ischemic myocardium so much lower than one might predict from the activity of the mitochondrial ATPase in sonicated heart mitochondria?

Journal of Molecular and Cellular Cardiology

Volumn 29, Issue 6, 1997, Pages 1505-1510

  Rouslin, W ^a   Long III, R B ^a   Broge, C W ^a  

^a UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; CREATINE PHOSPHATE; PROTON TRANSPORTING ADENOSINE TRIPHOSPHATE SYNTHASE;

CELL VIABILITY; EDITORIAL; ELECTRON TRANSPORT; ENZYME ACTIVITY; GLYCOLYSIS; HEART MITOCHONDRION; HEART MUSCLE ISCHEMIA; HEART PERFUSION; HEART RATE; HYDROLYSIS; MITOCHONDRIAL MEMBRANE; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PRIORITY JOURNAL;

EID: 0030910943     PISSN: 00222828     EISSN: None     Source Type: Journal    
DOI: 10.1006/jmcc.1997.0417     Document Type: Editorial

References (13)