Study of L-arginine in intestinal lesions caused by ischemia-reperfusion in rats (original) (raw)
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Transplantation Proceedings, 2008
Objective. Usualy an experimental necrotizing enterocolitis experimental model, we Investigated nitric oxide levels in intestinal tissues of newborn mice with or without L-arginine therapy during sessions of ischemia and reoxygenation. Methods. Twenty-six newborn mice from the Wistar EPM-1 lineage, weighing from 4.5 to 6.2 g, were randomly assigned to three groups: G-I/R, hypoxia and reoxygenation; G-Arg, L-arginine treatment I/R; and G-CTL, controls. G-I/R and G-Arg mice underwent twice a day during their first 3 days of life exposure to gas chambers with 100% CO 2 for 5 minutes at 22°C before reoxygenation with 100% O 2 for another 5 minutes. After 12 hours, all animals were sedated, laparotomized, and had samples of ileum and colon taken and-either formalin fixed histopathologic examations or frozen to Ϫ80°C for estimation of tissue nitric oxide levels. Intestinal injuries were classified according to the criteria of Chiu et al. Results. The G-I/R and G-Arg groups showed injuries characteristic of necrotizing enterocolitis (NEC) with an improved structural preservation rate in G-Arg. The concentration of nitric oxide in the Ileum was much higher with G-Arg (16.5 Ϯ 4.9; P ϭ 0.0019) G-I/R (7.3 Ϯ 2.0). This effect was not observed in the colon: G-I/R ϭ 10.7 Ϯ 4.6 versus G-Arg ϭ 15.5 Ϯ 8.7 (P ϭ .2480). Conclusion. Supply of L-arginine increased tissue levels of nitricoxide and reduced morphologic intestinal injury among mice undergoing I/R.
Protective Effects of L-Arginine on Rat Terminal Ileum Subjected to Ischemia/Reperfusion
Journal of Pediatric Gastroenterology and Nutrition, 2008
Objectives: Studies have shown that nitric oxide (NO) may play a major role in sustaining mucosal integrity; however, NO has been also implicated in the pathogenesis of ischemia/ reperfusion (I/R)-related tissue injury. We investigated the effects of L-arginine and N G-nitro L-arginine methyl ester (L-NAME) on the acetylcholine-induced contractile response of ileum and the levels of malondialdehyde (MDA) and reduced glutathione (GSH). Histopathological changes were also evaluated in ileal preparations. Materials and Methods: Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3 hours). Four groups were designed: shamoperated control; I/R; I/R and L-arginine pretreatment; and I/ R and L-NAME pretreatment. After reperfusion, ileum specimens were collected to determine the parameters mentioned above. Results: Following reperfusion, a significant decrease in acetylcholine-induced contractile response, an increase in lipid peroxidation, a decrease in GSH content, and mucosal damage of the ileal preparations were observed. We showed that decreased contractility, increased lipid peroxidation, and reduced GSH content have been reversed by L-arginine but not by L-NAME. Mucosal injury was significantly lowered in the L-arginine group. Conclusions: Treatment with L-arginine exerted a protective effect in intestinal I/R injury, which was mediated in part by regulating MDA and GSH levels, consequently ameliorating impaired contractile response and mucosal injury. JPGN 46:29-35, 2008.
Oral arginine improves intestinal recovery following ischemia-reperfusion injury in rat
Pediatric Surgery International, 2005
Arginine and nitric oxide are critical to the normal physiology of the gastrointestinal tract and maintain the mucosal integrity of the intestine in various intestinal disorders. In the present study, we evaluate the effects of oral arginine (ARG) supplementation on intestinal structural changes, enterocyte proliferation, and apoptosis following intestinal ischemia–reperfusion (IR) in the rat. Male Sprague–Dawley rats were divided into three experimental groups: sham rats underwent laparotomy and superior mesenteric artery mobilization, IR rats underwent superior mesenteric artery occlusion for 30 min following by 24 h of reperfusion, and IR-ARG rats were treated with enteral arginine given in drinking water (2%) 48 h before and following IR. Intestinal structural changes, enterocyte proliferation, and enterocyte apoptosis were determined 24 h following IR. A nonparametric Kruskal–Wallis ANOVA test was used for statistical analysis with p
Long-Term Enteral Arginine Supplementation in Rats with Intestinal Ischemia and Reperfusion
Journal of Surgical Research, 2012
Background. The effects of short-term enteral arginine supplementation on intestinal ischemiareperfusion (IR) injury have been widely studied, especially the ischemic preconditioning supplementation. The aim of this study was to investigate the effects of long-term intra-duodenal supplementation of arginine on intestinal morphology, arginine-associated amino acid metabolism, and inflammatory responses in rats with intestinal IR. Materials and Methods. Male Wistar rats with or without three hours of ileal ischemia underwent duodenal cannulation for continuous infusion of formula with 2% arginine or commercial protein powder for 7 d. The serological examinations, plasma amino acid and cytokine profiles, and intestinal morphology were assessed. Results. Intestinal IR injury had significant impacts on the decreases in circulating red blood cells, hemoglobin, ileum mass, and villus height and crypt depth of the distal jejunum. In addition, arginine supplementation decreased serum cholesterol and increased plasma arginine concentrations. In rats with intestinal IR injury, arginine supplementation significantly decreased serum nitric oxide, plasma citrulline and ornithine, and the mucosal protein content of the ileum. Conclusions. These results suggest that long-term intra-duodenal arginine administration may not have observable benefits on intestinal morphology or inflammatory response in rats with intestinal ischemia and reperfusion injury. Therefore, the necessity of long-term arginine supplementation for patients with intestinal ischemia and reperfusion injury remains questionable and requires further investigation.
Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury (II
Prostaglandins Leukotrienes and Essential Fatty Acids, 2001
Gastrointestinal mucosal blood flow is dependent on a balanced release of vasoactive substances from endothelium. Nitric oxide (NO) may increase the flow by vasodilatation and/or antiaggregation whereas endothelin (ET) may decrease it by vasoconstriction and aggregation. NO and ET may have counterbalancing effects on each other in tissue damage. In order to test this hypothesis, in this study on rats, L-arginine to increase NO levels and NG-nitro-L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/ reperfusion (I/R) injury model and portal vein ET response was evaluated. Lipid peroxidation product measurements and chemiluminescence (CL) studies were also carried out in ileal tissue samples. Intestinal I/R injury caused an increase in portal venous ET levels with levels of 9.4_+0.5 fmol/ml in sham operation and 14.8_+1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yielded the conclusion that inhibition of NO synthesis decreases portal venous ET levels in this model. Increased NO production by L-arginine caused increased ET levels in sham operated groups but this effect was not observed in I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under physiologic conditions and I/R injury.
Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury
Prostaglandins, Leukotrienes and Essential Fatty Acids, 1998
Gastrointestinal mucosal blood flow is dependent on a balanced release of vasoactive substances from endothelium. Nitric oxide (NO) may increase the flow by vasodilatation and/or antiaggregation whereas endothelin (ET) may decrease it by vasoconstriction and aggregation. NO and ET may have counterbalancing effects on each other in tissue damage. In order to test this hypothesis, in this study on rats, L-arginine to increase NO levels and NG-nitro-L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/ reperfusion (I/R) injury model and portal vein ET response was evaluated. Lipid peroxidation product measurements and chemiluminescence (CL) studies were also carried out in ileal tissue samples. Intestinal I/R injury caused an increase in portal venous ET levels with levels of 9.4_+0.5 fmol/ml in sham operation and 14.8_+1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yielded the conclusion that inhibition of NO synthesis decreases portal venous ET levels in this model. Increased NO production by L-arginine caused increased ET levels in sham operated groups but this effect was not observed in I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under physiologic conditions and I/R injury.
The Medical Journal of Cairo University, 2018
Background: Adropin is a peptide hormone that plays an important role in energy homeostasis and endothelial functions. Nitric oxide is a potent vasodilator synthesized in the vascular endothelium from the Nitric Oxide Synthase enzyme (NOS). There are controversial studies about the role of NOS and its isoforms the endothelial (eNOS) and the inducible (iNOS) forms in Ischemia-Reperfusion (IR) injury. It was found that adropin influences gene expression of eNOS and enhances endothelial cell function. However, few researchers have studied the link between adropin and iNOS activity during different phases of IR-injury. Aim of the Study: To estimate the plasma level of adropin, and iNOS activity and to study the relationship of both of them and their role during different phases of intestinal IRinjury in rats. Material and Methods: A total of 20 rats were used in this study (200-220g). Rats were divided into two groups (10 rats/each); group I (sham-operated group) and group II which exposed to laparotomy and occlusion of the superior mesenteric artery for 30min the reperfusion for 60min. Serial blood samples were taken via an inserted carotid catheter at 0, 30, and 90min. Plasma levels of adropin and iNOS were measured by ELISA kits according to the manufacturer protocols. The contents of the intestinal lumen were centrifuged and examined for detection of hemoglobin and albumin concentrations. ANOVA with a post hoc test, independent sample t-test, and Person correlation were used for statistical analyses. Results: Plasma adropin level and iNOS activity are significantly increased during ischemic and reperfusion phases of intestinal IR-injury when compared to the pre-ischemic phase of group II or when compared to the sham-operated group. Adropin was significantly correlated with iNOS during all phases. Moreover, unlike adropin, the iNOS level was correlated with the severity of the intestinal bleeding. Conclusion: Plasma adropin level is positively correlated with iNOS activity during different phases of intestinal IRinjury in rats, and this may provide new markers for diagnosis of IR-injury during intestinal surgeries.