OBJECTIVES: Sepsis is a common complication in the early postoperative period, leading to the augmentation of oxidative and nitrosative stresses. The present study investigated the role of enteral nutrition on nitric oxide (NO) production after a lipopolysaccharide (LPS)-induced endotoxemia as an index of nitrosative stress. METHODS: Fifty rats were subjected to midline laparotomy and feeding gastrostomy. Ten rats served as controls after recovering from operative stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo feeding for 24 h, after which they were injected intraperitoneally with LPS or equal volume of saline. Two hours later blood and liver tissue were collected. NO production was quantified in serum samples and homogenates of liver tissue by a modification of Griess's reaction. NO synthase (NOS) mRNA expression was examined in homogenate of liver tissue by reverse transcription-polymerase chain reaction. RESULTS: The operation significantly increased basal NO production in rat serum. LPS induced a further significant increase of NO levels. Enteral feeding of rats significantly decreased NO levels in both groups. In contrast, enteral nutrition was found to increase significantly NO levels in liver homogenates from rats treated with LPS. A constitutive endothelial NOS mRNA expression was found in liver tissue, whereas LPS administration induced inducible NOS mRNA expression in liver tissue regardless of enteral feeding. CONCLUSION: These findings indicate that early enteral feeding leads to a reduction in circulating NO levels induced by operation and endotoxemia, but increases hepatic NO levels in endotoxemia probably by the effect of LPS-induced inducible NOS on the increased L-arginine uptake.
OBJECTIVES: Sepsis is a common complication in the early postoperative period, leading to the augmentation of oxidative and nitrosative stresses. The present study investigated the role of enteral nutrition on nitric oxide (NO) production after a lipopolysaccharide (LPS)-induced endotoxemia as an index of nitrosative stress. METHODS: Fifty rats were subjected to midline laparotomy and feeding gastrostomy. Ten rats served as controls after recovering from operative stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo feeding for 24 h, after which they were injected intraperitoneally with LPS or equal volume of saline. Two hours later blood and liver tissue were collected. NO production was quantified in serum samples and homogenates of liver tissue by a modification of Griess's reaction. NO synthase (NOS) mRNA expression was examined in homogenate of liver tissue by reverse transcription-polymerase chain reaction. RESULTS: The operation significantly increased basal NO production in rat serum. LPS induced a further significant increase of NO levels. Enteral feeding of rats significantly decreased NO levels in both groups. In contrast, enteral nutrition was found to increase significantly NO levels in liver homogenates from rats treated with LPS. A constitutive endothelial NOS mRNA expression was found in liver tissue, whereas LPS administration induced inducible NOS mRNA expression in liver tissue regardless of enteral feeding. CONCLUSION: These findings indicate that early enteral feeding leads to a reduction in circulating NO levels induced by operation and endotoxemia, but increases hepatic NO levels in endotoxemia probably by the effect of LPS-induced inducible NOS on the increased L-arginine uptake.
Authors: Shermel B Sherman; Nadeen Sarsour; Marziyeh Salehi; Allen Schroering; Blair Mell; Bina Joe; Jennifer W Hill Journal: Gut Microbes Date: 2018-05-31