Gastrointestinal Transit during Endotoxemia: The Role of Nitric Oxide

Wirthlin, Douglas J.; Cullen, Joseph J.; Spates, Stephen T.; Conklin, Jeffrey L.; Murray, Joseph A.; Caropreso, David K.; Ephgrave, Kimberly S.

doi:10.1006/jsre.1996.0048

Cited by 82 publications

(59 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Then, the rats were killed by exsanguination 1 h later. Intestinal transit was determined by measuring the distance between the gastric pylorus and distal small intestine that was stained blue [13] .…”

Section: Intestinal Transitmentioning

confidence: 99%

“…MCP-1 is a potent chemoattractant that is capable o f p r o m o t i n g m o n o c y t e r e c r u i t m e n t i n t o a n inflammatory site, as well as activating monocytes and macrophages [29,30] . It has previously been shown that regulation of leukocyte recruitment and subsequent intestinal smooth muscle dysmotility during endotoxemia is mediated through MCP-1, and that a major source of MCP-1 is the dense network of resident muscularis macrophages [13] . In this study, we used MCP-1 mRNA as our marker of chemokine activity.…”

Section: N U M E R O U S S T U D I E S H Ave D E M O N S T R a T E D mentioning

confidence: 99%

See 1 more Smart Citation

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Yang¹,

Zhang²,

Sun³

et al. 2008

WJG

View full text Add to dashboard Cite

AIM:To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility. METHODS: Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS). Male Wistar ratswere randomly assigned to one of three treatment groups: magnolol prior to LPS injection (LPS/Mag group); vehicle prior to LPS injection (LPS/Veh group); vehicle prior to injection of saline (Control/Veh). Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), monocyte chemoattractant protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS) mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-κB (NF-κB) activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in the intestine 2 h after LPS injection. RESULTS:Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPStreated animals. TNF-α, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally, magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-κB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum. CONCLUSION: Magnolol prevents sepsis-inducedsuppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.

show abstract

Section: Intestinal Transitmentioning

confidence: 99%

Section: N U M E R O U S S T U D I E S H Ave D E M O N S T R a T E D mentioning

confidence: 99%

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Yang¹,

Zhang²,

Sun³

et al. 2008

WJG

View full text Add to dashboard Cite

show abstract

“…Endogenous cannabinoids have wide-ranging physiological activities, including the relaxation of intestinal smooth muscles [14][15][16] and vascular smooth muscles 2,16) . Both of these reponses are elicited by the CB1-R, but not the CB2-R. LPS is reported to induce the NO-mediated responses of decreased gastrointestinal transit 17) , and decreased ileal muscle contractility 18) and blood vessel relaxation 19) . Cytokine-induced microcirculation disorders 20) might be also involved in the intestinal relaxation and blood pressure reduction.…”

Section: Discussionmentioning

confidence: 99%

Rimonabant, a specific antagonist of the cannabinoid CB1-receptor, prevents lipopolysaccharide-induced endotoxemia in awake guinea pigs

Inagaki

Nemoto

Ninomiya

et al. 2010

Nihon Kyukyu Igakukai Zasshi

View full text Add to dashboard Cite

2-arachidonoyl glycerol (2-AG), an endogenous cannabinoid, has been drawing much attention as an early stage mediator at the onset of sepsis. In the present study, we investigated weather rimonabant, one of the CB1 antagonists, alleviated the medical conditions during endotoxemia and measured the level of prostaglandin E metabolite (PGEM). A cylindrical electric transmitter was connected to the transducer via a cable embedded beneath the animal's dorsal skin and sutured in place. Signals from the transmitter were detected by a receiver placed directly beneath the cage via telemetry. We monitored arterial pressure via catheter in the carotid artery and administrated drugs via catheter in jugular vein. We separated animals into three groups. The control group received lipopolysaccharide (LPS, 0.3 mg/kg, i.v.) and vehicle i.v. Experimental animals received LPS and rimonabant (1, 3 mg/kg/h) i.v. Ten minutes after the injection of the vehicle or rimonabant, LPS (0.3 mg/kg, i.v.) was administered. The prostaglandin E metabolites (PGEM) levels were measured by EIASA. In the control group, LPS induced intestinal paralysis and the decline in blood pressure peaked 1-3h after administration of LPS. In rimonabant-treated group, rimonabant inhibited LPS-induced intestinal paralysis and hypotension. Levels of PGEM in guinea pig was increased by LPS-administrate, rimonabant inhibits PGEM increase. The results suggest that rimonabant was effective against LPS-induced endotoxemia in guinea pigs. (JJAAM. 2010; 21: 118-25)

show abstract

“…Endotoxemia, which occurs after lipopolysaccharide (LPS) injection, delays gastric emptying and disrupts intestinal transit (1)(2)(3)(4)(5)(6)(7). However, it is not clear whether the latter effect involves a delay or acceleration since both have been reported (1,(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

“…However, it is not clear whether the latter effect involves a delay or acceleration since both have been reported (1,(5)(6)(7). While uncertainties remain about the nature of the effect of LPS on gastrointestinal motility, the effect is suspected to involve various cytokines that are produced in response to LPS (1)(2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Inducible nitric oxide synthase and tumor necrosis factor-alpha in delayed gastric emptying and gastrointestinal transit induced by lipopolysaccharide in mice

Inada¹,

Hamano²,

Yamada³

et al. 2006

Braz J Med Biol Res

View full text Add to dashboard Cite

Gastrointestinal motility disturbances during endotoxemia are probably caused by lipopolysaccharide (LPS)-induced factors: candidates include nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1ß, and interleukin-6. Flow cytometry was used to determine the effects of LPS and these factors on gastric emptying (evaluated indirectly by determining percent gastric retention; %GR) and gastrointestinal transit (GIT) in male BALB/c mice (23-28 g). NO (300 µg/mouse, N = 8) and TNF-α (2 µg/mouse, N = 7) increased (P < 0.01) GR and delayed GIT, mimicking the effect of LPS (50 µg/mouse). During early endotoxemia (1.5 h after LPS), inhibition of inducible NO synthase (iNOS) by a selective inhibitor, 1400 W (150 µg/mouse, N = 11), but not antibody neutralization of TNF-α (200 µg/mouse, N = 11), reversed the increase of GR (%GR 78.8 ± 3.3 vs 47.2 ± 7.5%) and the delay of GIT (geometric center 3.7 ± 0.4 vs 5.6 ± 0.2). During late endotoxemia (8 h after LPS), both iNOS inhibition (N = 9) and TNF-α neutralization (N = 9) reversed the increase of GR (%GR 33.7 ± 2.0 vs 19.1 ± 2.6% (1400 W) and 20.1 ± 2.0% (anti-TNF-α)), but only TNF-α neutralization reversed the delay of GIT (geometric center 3.9 ± 0.4 vs 5.9 ± 0.2). These findings suggest that iNOS, but not TNF-α, is associated with delayed gastric emptying and GIT during early endotoxemia and that during late endotoxemia, both factors are associated with delayed gastric emptying, but only TNF-α is associated with delayed GIT. Correspondence

show abstract

Gastrointestinal Transit during Endotoxemia: The Role of Nitric Oxide

Cited by 82 publications

References 3 publications

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Rimonabant, a specific antagonist of the cannabinoid CB1-receptor, prevents lipopolysaccharide-induced endotoxemia in awake guinea pigs

Inducible nitric oxide synthase and tumor necrosis factor-alpha in delayed gastric emptying and gastrointestinal transit induced by lipopolysaccharide in mice

Contact Info

Product

Resources

About