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mesenteric ischemia/arginiin
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Leht 1 alates 17 tulemused
The immune-enhancing enteral agents arginine and glutamine differentially modulate gut barrier function following mesenteric ischemia/reperfusion.
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BACKGROUND
Immune-enhancing enteral diets have been shown to improve patient outcome. One contributing mechanism may be via maintenance of gut barrier function. While recent data has shown that glutamine is beneficial, arginine may be harmful. We therefore hypothesized that the immune-enhancing
L-Arginine Modulates Intestinal Inflammation in Rats Submitted to Mesenteric Ischemia-Reperfusion Injury.
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The goal of this study was to investigate whether exogenous offer of L-arginine (LARG) modulates the gene expression of intestinal dysfunction caused by ischemia and reperfusion.
Eighteen Wistar-EPM1 male rats (250-300 g) were anesthetized and subjected to laparotomy. The superior mesenteric vessels
Protective effects of L-arginine on rat terminal ileum subjected to ischemia/reperfusion.
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OBJECTIVE
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 NG-nitro L-arginine methyl ester
Sustained nitric oxide production via l-arginine administration ameliorates effects of intestinal ischemia-reperfusion.
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BACKGROUND
The role of nitric oxide in intestinal ischemia-reperfusion is unclear-some studies link it to the harmful effects of ischemia-reperfusion, while others report it to be protective. We propose that nitric oxide levels diminish in the reperfusion period in conjunction with the onset of
L-Arginine and melatonin interaction in rat intestinal ischemia--reperfusion.
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We investigated the combinative effects of L-arginine and melatonin on the contractile responses of terminal ileum after the intestinal ischemia-reperfusion (I/R), in vivo. Male rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (180 min). We have observed a dramatic
Enteral arginine modulates inhibition of AP-1/c-Jun by SP600125 in the postischemic gut.
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We previously demonstrated that enteral arginine increased c-Jun/activator protein-1 (AP-1) DNA-binding activity and iNOS expression in a rodent model of mesenteric ischemia/reperfusion (I/R). The objective of this study was to specifically investigate the role of AP-1 in arginine's deleterious
Effect of N(G)-nitro-L-arginine methyl ester on intestinal permeability following intestinal ischemia-reperfusion injury in a rat model.
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Subclinical intestinal ischemia-reperfusion injury (IRI) causes an increase in mucosal permeability and may represent an early event in the pathogenesis of necrotizing enterocolitis in premature infants. Previous studies suggested that continuous, endogenous formation of nitric oxide (NO) maintains
Alterations of intestinal motor responsiveness in a model of mild mesenteric ischemia/reperfusion in rats.
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In this study we investigate the changes in intestinal motor responsiveness after mild mesenteric ischemia/reperfusion in anaesthetized rats. Motor responsiveness to pharmacological/electrical stimulation was studied in isolated ileum excised from sham-operated rats or animals which underwent
Pharmacologic treatment of occlusive mesenteric ischemia in rats.
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This study assessed the contribution of angiotensin II, oxygen-free radicals, and vasopressin to the mortality of acute mesenteric ischemia in rats. Rats received saline replacement (16 ml/kg/hr) for 3 hr during and after 85 min of superior mesenteric artery (SMA) occlusion. Only 21% of rats that
Possible relationship between histamine and nitric oxide release in the postischemic flow response following mesenteric ischemia of different durations.
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During the postischemic flow response (PFR), vasodilator mediators such as nitric oxide (NO) and histamine are liberated, influencing the blood flow rate at the onset of reperfusion. The possible roles of these two mediators, and the relationship between their release, were examined during segmental
Protective effect of leptin against ischemia-reperfusion injury in the rat small intestine.
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BACKGROUND
The small intestine is extremely sensitive to ischemia-reperfusion (I/R) injury and a range of microcirculatory disturbances which contribute to tissue damage. Previous studies have shown that leptin plays an important physiological role in the microvasculature. The aim of this study was
Vasopressin in vasodilatory and septic shock.
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OBJECTIVE
The aim of this article is to review mechanisms of action of vasopressin and clinical studies of vasopressin in septic shock.
RESULTS
Arginine vasopressin is an important stress hormone that has both vasoactive and antidiuretic properties. The vasoactive properties of vasopressin have been
Role of constitutive nitric oxide synthase and peroxynitrite production in a rat model of splanchnic artery occlusion shock.
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Peroxynitrite, a potent cytotoxic oxidant formed by the reaction of nitric oxide with superoxide anion, is an important mediator of reperfusion injury. In a rodent model of mesenteric ischemia and reperfusion injury we evaluated the contribution of the constitutive and/or inducible nitric oxide
Attenuated nitric oxide synthase activity and protein expression accompany intestinal ischemia/reperfusion injury in rats.
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Intestinal ischemia/reperfusion (I/R) leads to bowel impairment via the release of reactive oxygen species (ROS) and neutrophil infiltration. In addition to modulating intestinal integrity, nitric oxide (NO(*)) inhibits neutrophil activation and scavenges ROS. Attenuated endogenous NO(*) formation
Effect of hyperglycemia and nitric oxide synthase inhibition on heat tolerance and induction of heat shock protein 72 kDa in vivo.
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Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. Heat shock protein 72 (HSP-72) protects against KDa ischemia/reperfusion damage in vivo. The effect of diabetes on HSP-72 expression in vivo is unknown. The aim of this study was to determine
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- Korraldage oma huvisid ja hoidke end kursis uudisteuuringute, kliiniliste uuringute ja patentidega
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* Kogu teave põhineb avaldatud teaduslikel uuringutel
