Journal article
Myocardial energy metabolism and morphology in a canine model of sepsis
American journal of physiology. Heart and circulatory physiology, Vol.266(2), pp.H757-H768
02/01/1994
DOI: 10.1152/ajpheart.1994.266.2.H757
PMID: 8141377
Abstract
The mechanism responsible for sepsis-induced myocardial depression is not known. To determine if sepsis-induced myocardial depression is caused by inadequate free energy available for work, we studied myocardial energy metabolism in a canine model of sepsis. Escherichia coli-infected (n = 18) or sterile (n = 16) fibrin clots were implanted intraperitoneally into beagles. Myocardial function and structure was assessed using radionuclide ventriculograms, echocardiograms, and light and electron microscopy. The adequacy of energy metabolism was evaluated by comparing catecholamine-induced work increases [myocardial O2 consumption (MVO2) and rate pressure product (RPP)] with a simultaneously obtained estimate of intracellular free energy [phosphocreatine-to-adenosine triphosphate ratio (PCr:ATP)] determined by 31P-magnetic resonance spectroscopy. When compared with control animals, septic animals had a decrease in left ventricular ejection fraction (EF, P < 0.0001) on day 1 and fractional shortening (FS, P < 0.0003) on day 2 after clot implantation. On day 2, neither septic nor control animals had statistically significant decreases in PCr:ATP, despite catecholamine-induced increases in MVO2 and RPP (mean maximal increases in septic animals 135 +/- 31 and 51 +/- 10%, respectively). Light and electron microscopic findings showed that hearts of septic animals, compared with control animals, had a greater degree of morphological abnormalities. Thus, in a canine model of sepsis with alterations in myocyte ultrastructure and documented myocardial depression (decreased EF and FS), intracellular free energy levels (PCr:ATP) were maintained despite catecholamine-induced increases in myocardial work (increased MVO2 and RPP), suggesting high-energy synthetic capabilities are not limiting cardiac function.
Details
- Title: Subtitle
- Myocardial energy metabolism and morphology in a canine model of sepsis
- Creators
- Michael A Solomon - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Rosaly Correa - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892H Richard Alexander - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Lutchezar A Koev - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892J Perren Cobb - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892David K Kim - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892William C Roberts - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Zenaide M N Quezado - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Thomas D Scholz - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Robert E Cunnion - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892Willilam D Hoffman - Critical Care Medicine Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892John Bacher - National Heart Lung and Blood InstituteIdo Yatsiv - National Heart Lung and Blood InstituteRobert L Danner - National Heart Lung and Blood InstituteSteven M Banks - National Heart Lung and Blood InstituteVictor J FerransRobert S BalabanCharles Natanson - National Heart Lung and Blood Institute
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.266(2), pp.H757-H768
- DOI
- 10.1152/ajpheart.1994.266.2.H757
- PMID
- 8141377
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 02/01/1994
- Academic Unit
- Cardiology; Stead Family Department of Pediatrics; Child and Community Health
- Record Identifier
- 9984093476502771
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