Contributions of Leukocytes to Vascular Injury and Thrombosis
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Naturally occuring coronary reperfusion or reperfusion following treatment with fibrinolytic agents and/or percutaneous transluminal angioplasty can limit the extent of myocardial damage in patients with acute myocardial infarction (1–3). However, there are some undesirable sequelae of reperfusion which may limit its beneficial effects. One of these undesirable events is the acceleration of the acute inflammatory reaction observed in the early course of myocardial infarction (4–6). The contribution of the leukocytes which accumulate during this inflammatory response to myocardial damage and expansion of the infarct zone has been described (7,8). However, less attention has been directed to the early adherence of leukocytes to the vascular endothelium of the coronary vessels within the ischemic area. Accumulation of activated leukocytes on vascular endothelium could lead to several undesirable consequences relative to reflow to the ischemic area. These include physical obstruction of small vessels by leukocyte aggregates and thrombosis of both large and small vessels by direct endothelial cell injury or the generation of procoagulant substances (9–11). This paper will review the mechanisms by which PMN’s can initiate thrombosis of blood vessels at or near sites of tissue injury.
KeywordsPlatelet Activate Factor Leukocyte Adhesion Superficial Femoral Artery Ischemic Area PROCOAGULANT Activity
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