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Purpose: We aimed to investigate whether caffeic acid phenethyl ester (CAPE) prevents detrimental systemic effects of intestinal ischemia-reperfusion (IR) injury on colonic anastomotic wound healing. Methods: This experimental study was conducted on 48 male Wistar albino rats. The rats were randomly allocated into four groups and a left colonic anastomosis was performed in all rats: (i) sham-operated group (n = 12), laparatomy without intestinal IR injury; (ii) sham + CAPE group (n = 12), identical to Group 1 except for CAPE treatment (10 mu mol/kg, intravenously); (iii) intestinal IR group (n = 12), 60 min of superior mesenteric ischemia followed by reperfusion; and (iv) IR + CAPE-treated group (n = 12) (10 mu mol/kg, intravenously, 30 min before the construction of colonic anastomosis). On the postoperative day 7, the rats were subjected to relaparotomy for in vivo measurement of the colonic anastomotic bursting pressure. A colonic segment including the anastomotic site was resected for histopathological evaluation and biochemical analyses. The plasma proinflammatory cytokine levels were measured. Body weight changes were examined. Results: CAPE treatment significantly increased colonic anastomotic bursting pressures, and colonic anastomotic tissue hydroxyproline contents and antioxidant parameters (p < .05), and significantly decreased oxidative stress markers in colonic anastomotic tissues and plasma proinflammatory cytokine levels (p < .05). Histopathological scores were significantly better due to CAPE administration (p < .05). Conclusions: This study clearly showed that CAPE treatment prevented the delaying effects of remote IR injury on colonic anastomotic wound healing. Further clinical studies are required to determine whether CAPE has a useful role in the enhancement of gastrointestinal anastomotic wound healing during particular surgeries in which IR-induced organ injury occurs.

Purpose: We aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) on wound healing in left colonic anastomoses in the presence of intraperitoneal sepsis induced by cecal ligation and puncture (CLP) in a rodent model. Methods: This experimental study was conducted on 48 male Wistar albino rats. The animals were randomly allocated into four groups and a left colonic anastomosis was performed on the day following sham operation or CLP in all rats: (i) sham-operated control group, laparatomy plus cecal mobilization (n = 12) (Group 1), (ii) sham + CAPE group, identical to Group 1 except for CAPE treatment (10 mu mol/kg, intraperitoneally, 30 min before construction of the colonic anastomosis) (n = 12) (Group 2), (iii) CLP group, cecal ligation and puncture (n = 12) (Group 3), and (iv) CLP + CAPE-treated group, 10 mu mol/kg, intraperitoneally, 30 min before the construction of colonic anastomosis (n = 12) (Group 4). On the postoperative day 7, the animals were subjected to relaparotomy for in-vivo measurement of the colonic anastomotic bursting pressure. A colonic segment including the anastomotic site was resected for histopathological evaluation and biochemical analyses of hydroxyproline (Hyp) contents, myeloperoxidase (MPO) acivity, malondialdehyde (MDA) levels, reduced glutathione (GSH) levels, and superoxide dismutase (SOD) activity. Body weight changes were examined. Results: CAPE treatment significantly increased colonic anastomotic bursting pressures (p < .05), colonic anastomotic tissue Hyp contents, and enzymatic and nonenzymatic antioxidant markers (p < .05), and significantly decreased oxidative stress parameters in colonic anastomotic tissues (p < .05). Histopathological scores were significantly better by CAPE administration (p < .05). Conclusion: This study clearly showed that CAPE treatment prevented the detrimental effects of intraperitoneal sepsis on colonic anastomotic wound healing. Further clinical studies are required to determine whether CAPE has a useful role in the enhancement of gastrointestinal anastomotic wound healing during particular surgeries in which sepsis-induced organ injury occurs.

Background: This study was designed to determine the role of oxidative stress, nitric oxide (NO), and glutathione-related antioxidant enzymes in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury and to evaluate the potential benefits of prophylactic clarithromycin. Methods: One-day-old Wistar albino rat pups (N = 21) were randomly divided into 3 groups: group I (control), group II (exposed to H/R), and group III (clarithromycin + H/R). Clarithromycin was administered (40 mg/kg) subcutaneously to group III for 3 days. On the fourth day, all rats except controls were exposed to H/R and were killed at 6 hours after H/R. Histopathologic injury scores (HIS), malonyldialdehyde, glutathione (GSH), glutathione-peroxidase (GSH-Px) activities, and NO levels were measured on intestinal samples. Results: Whereas there was no difference for malonyldialdehyde levels among groups, HIS and NO levels were higher in group II than groups I and III (P < .05). However, GSH and GSH-Px activities were lower in group II than groups I and III (P < .05). Clarithromycin significantly increased GSH and GSH-Px activities and reduced HIS and NO levels in group III. Conclusion: This study showed that oxidative stress and NO contributed to the pathogenesis of H/R-induced bowel injury and that clarithromycin had a protective effect on bowel injury owing to antiinflammatory and antioxidant effects. (C) 2010 Elsevier Inc. All rights reserved.

INTRODUCTION: Pyrrolidine dithiocarbamate (PDTC) is a low-molecular thiol antioxidant and potent inhibitor of nuclear factor-kappaB (NF-kappaB) activation. In recent animal studies, the delaying effect of intraperitoneal sepsis on healing of colonic anastomoses has been demonstrated. In this study, we aimed to investigate the effects of PDTC on healing of colonic anastomoses in the presence of intraperitoneal sepsis induced by a rodent model of cecal ligation and puncture (CLP). METHODS: Anastomosis of the left colon was performed on the day following CLP in 30 rats that were divided into three groups: sham-operated control (laparotomy and cecal mobilization, group I, n =10), cecal ligation and puncture (CLP) (group II, n = 10), PDTC-treated group (100 mg/kg IV before construction of the colonic anastomosis) (group III, n = 10). On postoperative day 6, all animals were sacrificed, and anastomotic bursting pressures were measured in vivo. Tissue samples were obtained for further investigation of colonic anastomotic hydroxyproline (HP) contents, perianastomotic myeloperoxidase (MPO) activity, and malondialdehyde (MDA) and glutathione (GSH) levels. RESULTS: There was a statistically significant increase in the activity of MPO and MDA levels in the CLP group (group II) along with a decrease in GSH levels, colonic anastomotic HP contents, and bursting pressure values when compared to controls (group I). However, PDTC treatment led to a statistically significant increase in the tissue HP contents, GSH levels, and colonic anastomotic bursting pressure values, along with a decrease in MPO activity and MDA levels in group III (p < 0.05). CONCLUSIONS: This study showed that PDTC treatment significantly prevented the delaying effect of CLP-induced intraperitoneal sepsis on anastomotic healing in the colon. Further clinical studies are needed to clarify whether PDTC may be a useful therapeutic agent to increase the safety of the anastomosis during particular operations where sepsis-induced injury occurs.

Background and aims Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) is a water-soluble analogue of the spin label TEMPO. As an antioxidative agent, it is a member of nitroxides, which detoxifies superoxide and possibly other toxic radicals in vivo. In this study, we aimed to investigate whether tempol prevents harmful systemic effects of superior mesenteric ischemia-reperfusion on left colonic anastomosis in rats. Materials and methods Anastomosis of the left colon was performed in 30 rats that were divided into three groups each having ten animals: sham-operated control (group I), 60 min of intestinal ischemia-reperfusion by superior mesenteric artery occlusion (group II), and tempol-treated group (30 mg/kg before and after the ischemia-reperfusion (group III). On postoperative day 5, all animals were killed and anastomotic bursting pressures were measured in vivo. Tissue samples were obtained for further investigation of anastomotic hydroxyproline content, perianastomotic malondialdehyde, and glutathione levels. Results There was a statistically significant increase in the quantity of myeloperoxidase activity and malondialdehyde levels in group II, along with a decrease in glutathione levels, anastomotic hydroxyproline content, and bursting pressure values when compared to controls. However, all of the investigated parameters were normalized in tempol-treated animals (group III). Conclusion We conclude that tempol significantly prevents harmful systemic effects of reperfusion injury on colonic anastomoses in a rat model of superior mesenteric artery occlusion.

Introduction: Pyrrolidine dithiocarbamate (PDTC) is a low-molecular thiol antioxidant and potent inhibitor of nuclear factor-kappa B (NF-kappa B) activation. In recent animal studies, the delaying effect of intraperitoneal sepsis on healing of colonic anastomoses has been demonstrated. In this study, we aimed to investigate the effects of PDTC on healing of colonic anastomoses in the presence of intraperitoneal sepsis induced by a rodent model of cecal ligation and puncture (CLP). Methods: Anastomosis of the left colon was performed on the day following CLP in 30 rats that were divided into three groups: sham-operated control (laparotomy and cecal mobilization, group I, n = 10), cecal ligation and puncture (CLP) (group II, n = 10), PDTC-treated group (100 mg/kg IV before construction of the colonic anastomosis) (group III, n = 10). On postoperative day 6, all animals were sacrificed, and anastomotic bursting pressures were measured in vivo. Tissue samples were obtained for further investigation of colonic anastomotic hydroxyproline (HP) contents, perianastomotic myeloperoxidase (MPO) activity, and malondialdehyde (MDA) and glutathione (GSH) levels. Results: There was a statistically significant increase in the activity of MPO and MDA levels in the CLP group (group II) along with a decrease in GSH levels, colonic anastomotic HP contents, and bursting pressure values when compared to controls (group I). However, PDTC treatment led to a statistically significant increase in the tissue HP contents, GSH levels, and colonic anastomotic bursting pressure values, along with a decrease in MPO activity and MDA levels in group III (p < 0.05). Conclusions: This study showed that PDTC treatment significantly prevented the delaying effect of CLP-induced intraperitoneal sepsis on anastomotic healing in the colon. Further clinical studies are needed to clarify whether PDTC may be a useful therapeutic agent to increase the safety of the anastomosis during particular operations where sepsis-induced injury occurs.