Complement, neutrophils and free radicals: mediators of reperfusion injury.

@article{Lucchesi1994ComplementNA,
  title={Complement, neutrophils and free radicals: mediators of reperfusion injury.},
  author={Benedict Robert Lucchesi},
  journal={Arzneimittel-Forschung},
  year={1994},
  volume={44 3A},
  pages={420-32}
}
Myocardial ischemia of sufficient duration produces irreversible myocardial injury and cell death. Associated with the direct ischemic insult, there is the indirect attack on the jeopardized tissue through activation of the complement system. The latter, occurring in response to ischemia, facilitates neutrophil-endothelial cell interactions, neutrophil migration into and across the vascular wall, along with the formation of cytotoxic oxygen metabolites and release of proteolytic enzymes. The… CONTINUE READING

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Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Components of the complement system can damage tissue indirectly through formation of neutrophil chemoattractants as well as directly through assembly of the " membrane attack complex . "
Therefore , neutrophil - independent extension of irreversible cell death that occurs upon reperfusion , is additive to the component of cell death attributed to the ischemic interval .
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