title: Time course of necrosis/apoptosis and neovascularization during experimental gastric conditioning.
abstract: Apoptosis, necrosis and neovascularization are three processes that occur during ischemic preconditioning in a range of organs. In the stomach, the effect of this preconditioning (the delay phenomenon) has helped to improve gastric vascularization prior to esophagogastric anastomosis after esophagectomy. Here we present a sequential study of the histological recovery of the gastric fundus and the phenomena of apoptosis, necrosis and neovascularization in an experimental model of partial gastric ischemia. Partial gastric devascularization was performed by ligature of the left gastric vessels in Sprague-Dawley rats. Rats were assigned to groups in accordance with their evaluation period: control, 1, 3, 6, 10, 15 and 21 days. Histological analysis, caspase-3 activity, DNA fragmentation and vascular endothelial cell proliferation (Ki-67) were measured in tissue samples after sacrifice. After 24 h of partial gastric ischemia, rates of apoptosis and necrosis were higher in the experimental groups than in controls. Tissue injury was higher 3 and 6 days post-ischemia. From day 10 after partial gastric ischemia, apoptosis and necrosis started to decrease, and on days 15 and 21 showed no differences in relation to controls. Neovascularization began between days 1 and 3, reaching its peak at 15 days after ischemia and coinciding with complete histological recovery. Both necrosis and apoptosis play a role in tissue injury during the first days after partial gastric ischemia. After 15 days, the evolution of both the histology and the neovascularization suggested that this is the optimal time for performing gastric transposition.
authors.affiliation: Department of Surgery, Hospital Universitari de Bellvitge-Institut d'Investigació Biomédica de Bellvitge (IDIBELL), Barcelona, Spain.
authors.forename: S
authors.initials: S
authors.lastname: Lamas
authors.forename: D
authors.initials: D
authors.lastname: Azuara
authors.forename: J
authors.initials: J
authors.lastname: de Oca
authors.forename: M
authors.initials: M
authors.lastname: Sans
authors.forename: L
authors.initials: L
authors.lastname: Farran
authors.forename: E
authors.initials: E
authors.lastname: Alba
authors.forename: E
authors.initials: E
authors.lastname: Escalante
authors.forename: A
authors.initials: A
authors.lastname: Rafecas
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D004947:Esophagus / Q000098:blood supply / Q000601:surgery; D019194:Ischemic Preconditioning; D008297:Male; D009336:Necrosis; D009389:Neovascularization, Pathologic; D051381:Rats; D017207:Rats, Sprague-Dawley; D013270:Stomach / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology / Q000601:surgery