The proinflammatory cytokines TNF-α and IL-1β impair economy of contraction in human myocardium

Considerable experimental evidence has accumulated over the past years that proinflammatory cytokines, especially TNF-α and IL-1β, impair myocardial function in different animal species. On the other hand, several prospective clinical trials studying TNF-α antagonist in patients with chronic heart f...

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Bibliographic Details
Published in:Cytokine (Philadelphia, Pa.) Pa.), 2007-09, Vol.39 (3), p.157-162
Main Authors: Hofmann, U., Heuer, S., Meder, K., Boehler, J., Lange, V., Quaschning, T., Ertl, G., Bonz, A.
Format: Article
Language:English
Subjects:
Adult
Aged
Animals
Energy metabolism
Female
Humans
IL-1β
Inflammation Mediators - pharmacology
Interleukin-1beta - pharmacology
Isometric Contraction - immunology
Male
Middle Aged
Myocardial Contraction - immunology
Myocardium
Myocardium - immunology
Myocardium - metabolism
Oxygen Consumption - immunology
Proinflammatory cytokines
Rats
TNF-α
Tumor Necrosis Factor-alpha - pharmacology
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Summary:Considerable experimental evidence has accumulated over the past years that proinflammatory cytokines, especially TNF-α and IL-1β, impair myocardial function in different animal species. On the other hand, several prospective clinical trials studying TNF-α antagonist in patients with chronic heart failure were not able to demonstrate a benefit. As there might be a relevant species-related discrepancy, we intended to prove our previous results demonstrating impaired myocardial economy after exogenous administration of recombinant TNF-α in rat myocardium. In the present study, both TNF-α and IL-1β not only revealed an immediate negative inotropic effect but also increased specific oxygen demand in human right-atrial myocardium. Enhanced oxygen consumption was not caused by an elevated basal metabolism but an impaired economy of contraction. Our results suggest that proinflammatory cytokines have a considerable effect on myocardial mechano-energetic parameters in human myocardium as well.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2007.07.185