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Am J Physiol Regul Integr Comp Physiol 275: R502-R508, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 2, R502-R508, August 1998

TNF-alpha and myocardial depression in endotoxemic rats: temporal discordance of an obligatory relationship

Xianzhong Meng, Lihua Ao, Daniel R. Meldrum, Brian S. Cain, Brian D. Shames, Craig H. Selzman, Anirban Banerjee, and Alden H. Harken

Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado 80262

Exogenous tumor necrosis factor-alpha (TNF-alpha ) induces delayed myocardial depression in vivo but promotes rapid myocardial depression in vitro. The temporal relationship between endogenous TNF-alpha and endotoxemic myocardial depression is unclear, and the role of TNF-alpha in this myocardial disorder remains controversial. Using a rat model of endotoxemia not complicated by shock, we sought to determine 1) the temporal relationship of changes in circulating and myocardial TNF-alpha with myocardial depression, 2) the influences of protein synthesis inhibition or immunosuppression on TNF-alpha production and myocardial depression, and 3) the influence of neutralization of TNF-alpha on myocardial depression. Rats were treated with lipopolysaccharide (LPS, 0.5 mg/kg ip). Circulating and myocardial TNF-alpha increased at 1 and 2 h, whereas myocardial contractility was depressed at 4 and 6 h. Pretreatment with cycloheximide or dexamethasone abolished the increase in circulating and myocardial TNF-alpha and preserved myocardial contractile function. Similarly, treatment with TNF binding protein immediately after LPS prevented myocardial depression. We conclude that endogenous TNF-alpha mediates delayed myocardial depression in endotoxemic rats and that inhibition of TNF-alpha production or neutralization of TNF-alpha preserves myocardial contractile function in endotoxemia.

endotoxin; cardiac contractility; cycloheximide; dexamethasone; tumor necrosis factor binding protein; tumor necrosis factor-alpha


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