MYOCARDIAL ENERGY-METABOLISM AND MORPHOLOGY IN A CANINE MODEL OF SEPSIS

The mechanism responsible for sepsis-induced myocardial depression is not known. To determine if sepsis-induced myocardial depression is cau sed by inadequate free energy available for work, we studied myocardia l energy metabolism in a canine model of sepsis. Escherichia coli-infe cted (n = 18) or sterile (n = 16) fibrin clots were implanted intraper itoneally into beagles. Myocardial function and structure was assessed using radionuclide ventriculograms, echocardiograms, and light and el ectron microscopy. The adequacy of energy metabolism was evaluated by comparing catecholamine-induced work increases [myocardial O-2 consump tion (MVo(2)) and rate pressure product (RPP)] with a simultaneously o btained estimate of intracellular free energy [phosphocreatine-to-aden osine triphosphate ratio (PCr:ATP)] determined by P-31-magnetic resona nce spectroscopy. When compared with control animals, septic animals h ad a decrease in left ventricular ejection fraction (EF, P < 0.0001) o n day 1 and fractional shortening (FS, P < 0.0003) on day 2 after clot implantation. On day 2, neither septic nor control animals had statis tically significant decreases in PCr:ATP, despite catecholamine-induce d increases in MVo(2), and RPP (mean maximal increases in septic anima ls 135 +/- 31 and 51 +/- 10%, respectively). Light and electron micros copic findings showed that hearts of septic animals, compared with con trol animals, had a greater degree of morphological abnormalities. Thu s, in a canine model of sepsis with alterations in myocyte ultrastruct ure and documented myocardial depression (decreased EF and FS), intrac ellular free energy levels (PCr:ATP) were maintained despite catechola mine-induced increases in myocardial work (increased MVo(2), and RPP), suggesting high-energy synthetic capabilities are not limiting cardia c function.