Role of nitric oxide in gastrointestinal and hepatic function and disease

Stark, Mark E.; Szurszewski, Joseph H.

doi:10.1016/0016-5085(92)91454-c

Cited by 468 publications

(221 citation statements)

References 218 publications

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“…An attractive possibility is that LPS induces alterations in the paracrine control of gastric emptying via locally released cytokines. For instance, endotoxin-induced intestinal vascular damage is known to be mediated by cytokines such as nitric oxide, platelet-activating factor and thromboxane A2 (14). Alternatively, the LPS-induced gastric disturbance may be the result of an action of this bacterial endotoxin on specific areas of the CNS which control some of the gastric functions via the vagus nerve.…”

Section: Introductionmentioning

confidence: 99%

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Ef¹

1997

Braz J Med Biol Res

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The objectives of the present investigation were 1) to study the effect of bacterial lipopolysaccharide (LPS) on rat gastric emptying (GE) and 2) to investigate a possible involvement of the vagus nerve in the gastric action of LPS. Endotoxin from E. coli (strain 055:B5) was administered sc, ip or iv to male Wistar rats (220-280 g body weight) at a maximum dose of 50 µg/kg animal weight. Control animals received an equivalent volume of sterile saline solution. At a given time period after LPS administration, GE was evaluated by measuring gastric retention 10 min after the orogastric infusion of a test meal (2 ml/100 g animal weight), which consisted of 0.9% NaCl plus the marker phenol red (6 mg/dl). One group of animals was subjected to bilateral subdiaphragmatic vagotomy or sham operation 15 days before the test. A significant delay in GE of the test meal was observed 5 h after iv administration of the endotoxin at the dose of 50 µg/kg animal weight. The LPS-induced delay of GE was detected as early as 30 min and up to 8 h after endotoxin administration. The use of different doses of LPS ranging from 5 to 50 µg/kg animal weight showed that the alteration of GE was dose dependent. In addition, vagotomized animals receiving LPS displayed a GE that was not significantly different from that of the sham control group. However, a participation of the vagus nerve in LPS-induced delay in GE could not be clearly demonstrated by these experiments since vagotomy itself induced changes in this gastric parameter. The present study provides a suitable model for identifying the mechanisms underlying the effects of LPS on gastric emptyin

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Section: Introductionmentioning

confidence: 99%

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Ef¹

1997

Braz J Med Biol Res

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“…Nitric oxide (NO) is the principal inhibitory neurotransmitter in the gut, endothelial-derived NO is involved in the local regulation of mucosal blood flow and inflammatory-derived NO is involved in the loss of mucosal integrity [27,1]. Increased production of NO and subsequent local cytotoxicity to mucosal epithelial cells has been proposed as one of the putative mechanisms in the development of necrotizing enterocolitis (NEC) [6].…”

Section: Discussionmentioning

confidence: 99%

Interaction of Cholera Toxin B Subunit with Intestinal Epithelial Cells

Navolotskaya¹

2017

JED

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“…It should be noted that with systemic administration there is a possibility that some of the N OS inhibitor will be trapped in the liver (Stark and Szurszewski, 1992) as well as other systemic tissues, making it important to measure the degree of NOS inhibition directly. Systemic administration of L-NAME, however, induces marked increases in blood pres sure (Rees et aI., 1990), which can significantly alter the course of an ischemic insult and influence the degree of infarction.…”

Section: Discussionmentioning

confidence: 99%

Effects of Central Inhibition of Nitric Oxide Synthase on Focal Cerebral Ischemia in Rats

Hamada¹,

Greenberg²,

Croul

et al. 1995

J Cereb Blood Flow Metab

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Summary:We have investigated whether central inhibi tion of nitric oxide synthase (NOS) could modify the tis sue damage of focal cerebral ischemia produced by occlusion of the middle cerebral artery (MCA) in rats. �-Nitro-L-arginine methyl ester (L-NAME) was admin istered intracerebroventricularly at two doses 15 min prior to occlusion of the MCA, as well as 4 and 24 h following occlusion. After the injection of L-NAME, the catalytic activity of the constitutive NOS, considered to be mainly neuronal, was effectively suppressed in the sub cortical gray matter bilaterally, but not in the ischemic territory. Seven days after the MCA occlusion, the brains were evaluated for histopathologic damage. High-dose

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Role of nitric oxide in gastrointestinal and hepatic function and disease

Cited by 468 publications

References 218 publications

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

Interaction of Cholera Toxin B Subunit with Intestinal Epithelial Cells

Effects of Central Inhibition of Nitric Oxide Synthase on Focal Cerebral Ischemia in Rats

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