Key result
Activation of human neutrophils with hrC5a provoked reduction in myocardial contractility, which was significantly attenuated by pretreatment with antibodies to the CD18 adhesion complex.
Why the study?
Does activation of human neutrophils by hrC5a reduce the contractile function of isolated rabbit papillary muscles, and is this dependent on the CD18 adhesion complex?
Does activation of human neutrophils by hrC5a reduce the contractile function of isolated rabbit papillary muscles, and is this dependent on the CD18 adhesion complex?
Activated human neutrophils impair myocardial contractility via CD18 complex-dependent adhesion, suggesting a mechanism for leukocyte-mediated myocardial injury.
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Kraemer et al. (1991) studied this question. Human neutrophils activated by human recombinant C5a (hrC5a) with or without pretreatment with monoclonal antibodies to the CD18 adhesion complex vs. Neutrophils alone or hrC5a alone was evaluated on Changes in papillary muscle function (myocardial contractility). Activation of human neutrophils with hrC5a provoked reduction in myocardial contractility, which was significantly attenuated by pretreatment with antibodies to the CD18 adhesion complex.
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