(Circulation. 1997;95:778-781.)
© 1997 American Heart Association, Inc.
Articles |
Cytokines and Cardiac Contractile Function
the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.
Correspondence to Ralph A. Kelly, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail rakelly@bics.bwh.harvard.edu.
Key Words: Editorials • heart failure • cytokines • nitric oxide • myocarditis
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Introduction |
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A working understanding of the molecular and cell biology of inflammatory cytokines is of growing importance to both cardiovascular scientists and practicing clinicians. Accumulating evidence indicates that these locally acting polypeptide mediators, or "autacoids," play a role not only in the pathogenesis of atherosclerosis and in the cardiac dysfunction that accompanies systemic sepsis, viral myocarditis, and cardiac allograft rejection but also in advanced heart failure syndromes resulting from diverse pathogenic insults. ("Autacoid" is derived from the Greek words autos ["self"] and akos ["remedy"]; autacoids are locally acting, biologically active agents [both peptides and nonpeptides] that are distinct from neurotransmitters and hormones in the circulation.1 ) More than 25 years ago, Lefer and Rovetto2 reported that the sera of septic patients and experimental animals contained a "myocardial depressant factor," the molecular nature of which has eluded definitive identification in the intervening years. During the past decade, Parrillo and colleagues3 4 used intact animals and in vitro isolated heart cell preparations to systematically investigate the factors that contribute to myocardial depression in systemic sepsis (ie, the systemic inflammatory response syndrome) and concluded that TNF-
and IL-1ß were shown to be present in the sera of septic patients and are responsible for most, if not all, of the reversible cardiac depression often seen with this syndrome. These data are consistent with earlier reports (reviewed in Levine et al5 ) that soluble inflammatory mediators in medium conditioned by activated immunocytes altered the contractile responsiveness of beating cardiac muscle cells to ß-adrenergic agonists, an effect that This article has been cited by other articles:
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