title: Vitamin E prevents neutrophil accumulation and attenuates tissue damage in ischemic-reperfused human skeletal muscle.
abstract: Neutrophil accumulation and the consequent production of oxygen-derived free radicals are involved in the pathogenesis of Ischemia-Reperfusion syndrome. In this study we investigated whether a treatment with Vitamin E, which has antioxidant properties, could attenuate the tissue damage by interfering with the influx of neutrophils within the ischemic and reperfused human skeletal muscle. To this purpose, patients undergoing aortic cross-clamping during the surgical repair of aortic abdominal aneurysm were studied as a model of ischemia-reperfusion of the lower limb muscles. Muscle biopsies from the right femoral quadriceps of patients not receiving and receiving Vitamin E pretreatment before surgery were taken: a) after the induction of anaesthesia, as control samples, and b) after a period of ischemia followed by 30 min of reperfusion. The tissue samples were either routinely processed for morphological study and immunohistochemical analysis to detect an altered expression of specific endothelial adhesion proteins, such as E-selectin and ICAM-1. The results obtained showed that Vitamin E administration was able to prevent the accumulation of neutrophils within the ischemic and reperfused muscle. This beneficial effect of Vitamin E was due to its ability to hinder the expression of E-selectin and ICAM-1, molecules known to increase the adhesiveness of endothelium to circulating neutrophils. After treatment with Vitamin E a marked attenuation of the reperfusion injury was also evident. In conclusion, Vitamin E treatment may be considered a valuable tool for protection against the ischemia-reperfusion damage of human skeletal muscle.
authors.affiliation: Department of Human Anatomy and Histology, University of Florence, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Formigli
authors.forename: L
authors.initials: L
authors.lastname: Ibba Manneschi
authors.forename: A
authors.initials: A
authors.lastname: Tani
authors.forename: E
authors.initials: E
authors.lastname: Gandini
authors.forename: C
authors.initials: C
authors.lastname: Adembri
authors.forename: C
authors.initials: C
authors.lastname: Pratesi
authors.forename: G P
authors.initials: GP
authors.lastname: Novelli
authors.forename: S
authors.initials: S
authors.lastname: Zecchi Orlandini
mesh_terms: D000368:Aged; D019040:E-Selectin / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects* / Q000648:ultrastructure; D009504:Neutrophils / Q000187:drug effects*; D015427:Reperfusion Injury / Q000378:metabolism*; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D019040:E-Selectin; D018799:Intercellular Adhesion Molecule-1; D014810:Vitamin E