Supplementation with high-dose ascorbic acid improves intestinal anastomotic healing.

BACKGROUND/AIM: Ascorbic acid modulates tissue healing but the value of ascorbic acid supplementation during anastomotic healing remains unclear. We examined the role of ascorbic acid treatment in experimental intestinal resection. METHODS: Male Wistar albino rats (n = 30) were divided into three groups: sham treatment (group 1), and daily ascorbic acid treatment with 100 mg/kg (group 2) or 200 mg/kg (group 3) via the intramuscular route. Following sacrifice on the 7th postoperative day, bursting pressure of the anastomoses was measured. Hydroxyproline assessment and histological analysis were carried out. RESULTS: The bursting pressure values of groups 2 (171.4 +/- 4.3 mm Hg) and 3 (196.4 +/- 2.2 mm Hg) were higher than that of group 1 (139.1 +/- 4.1 mm Hg; p < 0.05). In addition, the hydroxyproline level of group 3 (249.2 +/- 25.1 microg/mg) was higher than that of groups 1 (157.9 +/- 14.9 microg/mg) and 2 (187.9 +/- 14.8 microg/mg; p < 0.05). The histopathological scores indicated improved healing in groups 3 (6.0 +/- 0.2) and 2 (4.4 +/- 0.4), compared to group 1 (2.7 +/- 0.3; p < 0.05). CONCLUSION: In the present study, supraphysiologic doses of ascorbic acid improved anastomotic healing. Therefore, vitamin C supplementation poses as a beneficial treatment in the context of collagen accumulation, inflammatory response, and anastomotic strength. However, the clinical value of high-dose ascorbic acid supplementation in the clinical setting is yet to be established.

Nitric oxide as an independent regulatory factor in regenerating rat liver.

Nitric oxide production and lipid peroxidation modulate the proliferating activity of liver cells, but the relationship between enhanced nitric oxide production, lipid peroxidation, and liver regeneration remains unclear. We examined the role of nitric oxide and lipid peroxidation on experimental liver regeneration. Thirty-five male Wistar albino rats underwent a sham operation (I), partial hepatectomy alone (II, IV), partial hepatectomy and daily N-nitro-L-arginine methyl ester (L-NAME) treatment for 24-hrs (III) or 48-hrs (V). Liver tissue concentrations of catalase, nitrite and nitrate, glutathione, and serum levels of alaninaminotransferase and bilirubin were measured. CD34, Ki-67 and proliferating cell nuclear antigen were evaluated in liver samples. Compared with other groups, both of the L-NAME groups had decreased tissue nitric oxide concentrations. Nitrate and nitrite (nitric oxide) concentrations were higher in partial hepatectomy-alone groups, as were CD34 counts and proliferation indexes. Partial hepatectomy elevated catalase, and glutathione levels in all groups compared to the sham-operated controls. In conclusion, nitric oxide inhibition impaired hepatic regeneration following partial hepatectomy. An obvious effect of nitric oxide on lipid peroxidation in the context of hepatocyte and endothelial cell proliferation could not be demonstrated. Thus, while lipid peroxidation could influence some steps in liver regeneration, nitric oxide poses as an independent regulatory factor in regenerating rat liver.

The effects of nitric oxide supplementation and inhibition on bacterial translocation in bile duct ligated rats.

Obstructive jaundice promotes bacterial translocation from the gut, but the role of nitric oxide is controversial in this process. We studied the effects of nitric oxide synthase substrate, L-arginine, and nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester, on bacterial translocation in bile duct ligated rats. The animals were randomized into five groups; control, sham, common bile duct ligation alone, nitric oxide inhibition, and nitric oxide supplementation. Obstructive jaundice was performed with common bile duct ligation. L-arginine or N(G)-nitro-L-arginine methyl ester was injected once daily for 14 days. Blood bilirubin level, liver histology, and bacterial translocation to the mesenteric lymph nodes as well as to the liver were assessed. The L-arginine supplemented group had the lowest bacterial translocation rate, but the most prominent hepatic fibrosis. Nitric oxide inhibition increased bacterial translocation to the mesenteric lymph nodes. Therefore, the administration of nitric oxide donor or inhibitor acts as a significant regulatory factor for bacterial translocation in obstructive jaundice.

Effect of granulocyte-macrophage colony stimulating factor on bacterial translocation after experimental obstructive jaundice.

OBJECTIVE: To investigate the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on bacterial translocation promoted by obstructive jaundice. DESIGN: Controlled animal study. SETTING: University hospital, Turkey. ANIMALS: 30 male Wistar albino rats. INTERVENTIONS: The first group (n = 10) was the sham operation (control) group, and the second and the third (n = 10 each) had common bile duct (CBD) ligation and division under sterile conditions. The third group were also treated with GM-CSF 200 ng subcutaneously daily between the fifth and ninth postoperative days. All animals were killed on the tenth day, and evaluated biochemically and histopathologically. Mesenteric lymph nodes were cultured under aerobic conditions. MAIN OUTCOME MEASURES: Biochemical analysis, histopathological evaluation, and aerobic cultures. RESULTS: There was no bacterial translocation in either the control or GM-CSF groups, whereas Escherichia coli and Salmonella typhimurium were found in 4 and 2 animals, respectively in the ligation group. Although no aerobic bacteria was found in controls and the GM-CSF groups, bacterial translocation was 6/10 in the ligation alone group (p <0.01). CONCLUSION: Activation of inflammatory response with GM-CSF is highly effective in prevention of bacterial translocation in obstructive jaundice.