title: Intestinal ischemic preconditioning protects the intestine and reduces bacterial translocation.
abstract: Ischemic preconditioning (IPC) was first demonstrated in the heart, but this protective effect has been also recently described in the intestine. The aim of this study was to determine the effects of intestinal ischemic preconditioning on the morphology of intestine and bacterial translocation. Twenty-four male Wistar rats weighting 250 to 300 g were randomized into three groups. A control group of rats (n = 8) were subjected laparotomy. In an ischemic group (n = 8), laparotomy was performed and the superior mesenteric artery was occluded by an atraumatic clamp for 30 min. In the preconditioned group (n = 8), before the ischemia-reperfusion (I/R) period (as in ischemic group), rats were subjected to an initial 10 min of intestinal ischemia and 10 min of reperfusion. Twenty-four hours later, to evaluate whether the I/R induced intestinal injury and bacterial translocation (BT), tissue and blood samples were collected, and liver, spleen, and mesenteric lymph node specimens were obtained under sterile conditions for microbiological analysis. Samples of ileum were removed for both biochemical and histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, liver, and blood was significantly higher than other groups (P < 0.05). IPC prevented I/R-induced BT and it significantly reduced the I/R-induced intestinal injury (P < 0.05). Increased inducible nitric oxide (NO) synthase (iNOS) expression observed on the ileal specimens of the I/R group was found to be prevented by IPC. Our data suggest IPC as a key factor that reduces BT and iNOS activation in intestinal I/R. This is the first study showing that intestinal IPC blocks the cascade of events that causes BT and intestinal injury that may lead to sepsis.
authors.affiliation: Department of Pediatric Surgery, Mersin University School of Medicine, Turkey.
authors.forename: Selim
authors.initials: S
authors.lastname: Aksöyek
authors.forename: Ismail
authors.initials: I
authors.lastname: Cinel
authors.forename: Dinçer
authors.initials: D
authors.lastname: Avlan
authors.forename: Leyla
authors.initials: L
authors.lastname: Cinel
authors.forename: Candan
authors.initials: C
authors.lastname: Oztürk
authors.forename: Polat
authors.initials: P
authors.lastname: Gürbüz
authors.forename: Ali
authors.initials: A
authors.lastname: Nayci
authors.forename: Uğur
authors.initials: U
authors.lastname: Oral
mesh_terms: D000818:Animals; D004926:Escherichia coli / Q000302:isolation & purification; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D019194:Ischemic Preconditioning; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000378:metabolism / Q000382:microbiology / Q000473:pathology / Q000517:prevention & control
chemical_list: D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat