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pubmed:abstractText |
In addition to their traditional role in infection elimination and scavenging dead tissue, neutrophils may be injurious to myocardial tissues. Besides mechanical participation they produce toxic oxygen species, PAF, arachidonic acid metabolites, and release the proteases from intracellular granules. The deleterious role of PMN within myocardial ischemic focus depends also on the cooperation with platelets, macrophages, endothelial and mast cells. Rapid entry of neutrophils during ischemia contribute to arrhythmia, loss of coronary vasomotion, no-reflow phenomenon and extension of cellular injury. Further work is needed to define the precise role that neutrophils play in tissue injury and to propose an appropriate strategy by which PMN function can be modified to limit infarct size.
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