title: Expression of E-selectin on coronary endothelium after myocardial ischemia and reperfusion.
abstract: Neutrophils localize in ischemic or infarcted myocardium and thus are implicated in playing a role in myocardial reperfusion injury and stunning. We studied one of the mechanisms by which neutrophils are recruited into the region of ischemic myocardium. Anesthetized adult rhesus monkeys (n = 2) underwent ligation of one of the obtuse marginal coronary arteries for 90 minutes followed by 5 hours of reperfusion. Tissues from the normal perfused area of the heart and from the ischemic area were preserved in methacarn fixative after sacrificing the animal at the end of the reperfusion period. Immunohistochemical staining showed that E-selectin is not constitutively expressed on coronary endothelium in vivo. E-selectin, however, was upregulated in selective endothelial cells located in the postcapillary coronary venules in response to ischemia and reperfusion. The presence of E-selectin in this setting suggests that it may have a similar role as in the recruitment of neutrophils into other inflamed or damaged tissues.
authors.affiliation: Division of Cardiothoracic Surgery, University of Washington, Seattle.
authors.forename: I
authors.initials: I
authors.lastname: Shen
authors.forename: E D
authors.initials: ED
authors.lastname: Verrier
mesh_terms: D000818:Animals; D002448:Cell Adhesion / Q000502:physiology*; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000502:physiology*; D002634:Chemotaxis, Leukocyte; D019040:E-Selectin; D004727:Endothelium / Q000737:chemistry; D007124:Immunoenzyme Techniques; D008253:Macaca mulatta; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D017682:Myocardial Stunning / Q000503:physiopathology*; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D009504:Neutrophils / Q000502:physiology*; D011971:Receptors, Immunologic / Q000502:physiology*
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D011971:Receptors, Immunologic