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Polymorphonuclear leukocytes reduce cardiac function in vitro by release of H2O2
R Kraemer1, B Seligmann, K M Mullane
1Department of Pharmacology, New York Medical College, Valhalla 10595.
The American Journal of Physiology
|June 1, 1990
Summary
Polymorphonuclear leukocytes (PMNs) impair cardiac function by releasing hydrogen peroxide (H2O2). This study shows PMNs significantly decrease contractile force in isolated heart muscles, with H2O2 identified as the primary mediator.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Inflammation Research
Background:
- Polymorphonuclear leukocytes (PMNs) are linked to myocardial injury after ischemia.
- Understanding PMN's direct impact on cardiac contractility is crucial.
Purpose of the Study:
- To investigate the direct effects of PMNs on cardiac contractile function.
- To identify the specific mechanisms by which PMNs induce cardiac dysfunction.
Main Methods:
- Isolated rabbit right ventricular papillary muscles were exposed to varying concentrations of purified PMNs.
- Contractile function was measured, and the role of reactive oxygen species was assessed using scavengers and direct hydrogen peroxide (H2O2) exposure.
Main Results:
- PMNs caused a concentration-dependent reduction in papillary muscle contractile force and its derivatives.
- PMN-induced dysfunction correlated with PMN activity.
- Catalase attenuated the contractile loss, while superoxide dismutase did not. Direct H2O2 exposure mimicked PMN effects.
Conclusions:
- PMNs likely reduce cardiac contractile function through the release of hydrogen peroxide (H2O2).
- H2O2 is a key mediator of PMN-induced cardiac dysfunction in this model.