Neutrophils and myocardial reperfusion injury.
Ischaemia induces an acute inflammatory response in myocardial tissue with an early phase of neutrophil accumulation, which is accelerated by reperfusion. In experimental models, interventions that deplete neutrophils or inhibit their function cause a significant reduction in myocardial infarct size. These cells, therefore, may exacerbate tissue injury through the release of free radicals and proteolytic enzymes. Neutrophil recruitment depends on the presence of inflammatory mediators. Leukotriene B4, interleukin 8 and the complement fragment C5a have been implicated in this process. Studies using antibodies to the selectin, integrin and immunoglobulin superfamily adhesion molecules indicate that they also have a crucial role in myocardial neutrophil recruitment.
Williams
F M
FM
Applied Pharmacology, National Heart And Lung Institute, Imperial College of Science, Technology and Medicine, London, UK.
D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000187:drug effects; D015936:Complement C5a / Q000378:metabolism; D004195:Disease Models, Animal; D005609:Free Radicals; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D007975:Leukotriene B4 / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000503:physiopathology; D009504:Neutrophils / Q000166:cytology / Q000473:pathology*; D010972:Platelet Activating Factor / Q000378:metabolism
D000906:Antibodies; D015815:Cell Adhesion Molecules; D005609:Free Radicals; D016209:Interleukin-8; D010972:Platelet Activating Factor; D007975:Leukotriene B4; D015936:Complement C5a