Amplification of the inflammatory response: adhesion molecules associated with platelet/white cell responses
Abstract
Cardiopulmonary bypass (CPB) causes leukocyte and platelet activation, resulting in upregulation of the adhesion receptor CD11b/CD18 on leukocytes and upregulation of P-selectin, the adhesion receptor that binds the activated platelet to polymorphonuclear neutrophils (PMNs) and monocytes. Our laboratory has studied the expression of activation-dependent adhesion receptors during in vivo CPB. Both PMN and monocyte CD11b were upregulated during CPB but with differing time courses. Peak PMN CD11b levels occurred at the end of the hypothermic phase of bypass, whereas monocyte CD11b levels increased steadily throughout the course of CPB, peaked at 2-4 h after CPB, and remained significantly elevated as late as 18-24 h post CPB. The percentage of P-selectin-positive platelets increased significantly during bypass, peaking around the end of bypass and remaining elevated in the early post-bypass period. The level then returned to normal by 18 h post-bypass. Monocyte-platelet binding paralleled the increase in P-selectin-positive platelets during bypass and similarly remained elevated in the post-bypass period. PMN-platelet binding also increased but peaked early during CPB. Upregulation of these adhesive receptors and formation of plat...Continue Reading
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Sodium nitroprusside during coronary artery bypass grafting: evidence for an antiinflammatory action
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