EXPRESSION OF E-SELECTIN IN ISCHEMIC AND REPERFUSED HUMAN SKELETAL-MUSCLE

Citation
L. Formigli et al., EXPRESSION OF E-SELECTIN IN ISCHEMIC AND REPERFUSED HUMAN SKELETAL-MUSCLE, Ultrastructural pathology, 19(3), 1995, pp. 193-200
Citations number
32
Categorie Soggetti
Microscopy,Pathology
Journal title
ISSN journal
01913123
Volume
19
Issue
3
Year of publication
1995
Pages
193 - 200
Database
ISI
SICI code
0191-3123(1995)19:3<193:EOEIIA>2.0.ZU;2-R
Abstract
This work was undertaken to assess the role of endothelial E-selectin in the development of neutrophil accumulation into the ischemic and re perfused human skeletal muscle and eventually in the genesis of ischem ia-reperfusion syndrome. Twelve patients affected by abdominal aortic aneurysm who were undergoing reconstructive vascular surgery were stud ied. Muscle biopsies from the right femoral quadriceps were taken (1) immediately after anesthesia, as control samples, (2) before declampin g the aorta, as ischemic samples, and (3) 30 minutes after reperfusion and then processed for immunohistochemical and ultrastructural analys is. Immunohistochemistry revealed a strong positive reaction for E-sel ectin on the venular endothelium during ischemia and reperfusion. Ultr astructural investigation showed that reactivity for E-selectin matche d neutrophil accumulation of the skeletal muscle tissue. This phenomen on was dependent upon a complex series of events that included neutrop hil adhesion to the inner surface of the postcapillary venules, passag e through endothelial intercellular junctions, and migration distally into the interstitial spaces of the skeletal muscle tissue. Neutrophil tissue infiltration was also associated with ultrastructural signs of tissue damage at reperfusion. This is in agreement with accumulating evidence indicating a role for tissue infiltrating neutrophils in the genesis of toxic O-2 free radicals. Our data suggest that E-selectin e xpression on the vascular endothelium of human skeletal muscle may rep resent a key regulatory point in the process of neutrophil tissue accu mulation and indicate an active role for the venular endothelium in th e development of human ischemia-reperfusion syndrome.