Gastric nitric oxide synthase expression during endotoxemia: Implications in mucosal defense in rats

Helmer, Kenneth S.; West, Sonlee D.; Shipley, Gregory L.; Chang, Lily; Cui, Yan; Mailman, David; Mercer, David

doi:10.1053/gast.2002.34178

Cited by 41 publications

(71 citation statements)

References 32 publications

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“…Evaluation of gastric luminal nitrate and nitrite levels, another measure of NO, is also increased after 1 h of LPS treatment. Unlike the bladder, however, up-regulation of NO may be due to increases in iNOS because Ca 2ϩ -independent, but not Ca 2ϩ -dependent NOS activity, is elevated in gastric mucosa after 1 h of LPS treatment (Helmer et al, 2002). In the mouse bladder, after 1 h of treatment with LPS, we found an increase in Ca 2ϩ -dependent but not Ca 2ϩ -independent NOS activity.…”

Section: Enos Up-regulation In Lps-induced Mouse Bladder Inflammationcontrasting

confidence: 51%

Rapid Up-Regulation of Endothelial Nitric-Oxide Synthase in a Mouse Model ofEscherichia coliLipopolysaccharide-Induced Bladder Inflammation

Kang¹,

Tamarkin²,

Wheeler³

et al. 2004

J Pharmacol Exp Ther

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Increases in the signaling molecule nitric oxide (NO) during inflammation may be linked not only to inducible nitric-oxide synthase (iNOS) but also to endothelial (e)NOS. Escherichia coli lipopolysaccharide (LPS) induces an inflammatory response in the bladder and rapidly increases phosphorylation of Akt/protein kinase B (Akt), a key enzyme regulating proliferation, apoptosis, and inflammation. Activated Akt phosphorylates human eNOS at serine 1177 and subsequently increases NOS activity. Because Akt and eNOS are both localized in the bladder urothelium, phosphorylation of eNOS by Akt provides an attractive mechanism for rapid increases in urinary NO production. Female mice were intraperitoneally injected with LPS (25 mg/kg) or pyrogen-free water (control). Four hours before LPS injection, some mice were injected with wortmannin, which inhibits Akt phosphorylation. Levels of urinary cyclic GMP, a downstream product of NO, increase 75% within 1 h after intraperitoneal injection of LPS, and this increase is blocked by wortmannin. Bladder eNOS and phosphorylated eNOS protein increase 94 and 151%, respectively, 1 h after LPS treatment, whereas iNOS was not detected. Wortmannin decreases eNOS phosphorylation by 60%. Furthermore, bladder Ca 2ϩ -dependent NOS activity (eNOS, neuronal NOS) is increased 79 Ϯ 20% 1 h after LPS treatment, whereas there is no increase in Ca 2ϩ -independent (iNOS) activity (n ϭ 4). Increases in urinary cyclic GMP, NOS activity, and eNOS protein and phosphorylation 1 h after induction of inflammation with LPS, indicate that eNOS plays a role in the early response to bladder inflammation.

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Section: Enos Up-regulation In Lps-induced Mouse Bladder Inflammationcontrasting

confidence: 51%

Rapid Up-Regulation of Endothelial Nitric-Oxide Synthase in a Mouse Model ofEscherichia coliLipopolysaccharide-Induced Bladder Inflammation

Kang¹,

Tamarkin²,

Wheeler³

et al. 2004

J Pharmacol Exp Ther

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“…In addition, LPS disrupted gastric F-actin cytoskeletal components indicative of injury to the sub-cellular architecture of the gastric epithelium. These data indicated that LPS not only caused gastric injury when given alone, but also exacerbated gastric injury from the luminal irritant bile according to macroscopic, morphologic, and sub-cellular criteria [15] .…”

Section: Introductionmentioning

confidence: 82%

“…LPS both time and dose dependently exacerbated gastric injury from bile when compared to control rats [15] . Histologically, LPS in the absence of bile was found to cause injury to primarily the surface epithelial cells and gastric pits.…”

Section: Introductionmentioning

confidence: 88%

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The Gut in Systemic Inflammatory Response Syndrome and Sepsis

et al. 2007

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The prognosis and care of critically ill ICU patients has improved over recent years, but the development of multiple organ failure (MOF) continues to cause significant morbidity and mortality. Shock, with resultant organ ischemia, appears to play a critical role in the development of MOF. It is our global hypothesis that MOF is a gut-derived phenomenon and that novel interventions can improve outcome in shock-induced gut inflammation and dysfunction in critically ill patients. We have found that the anesthetic agent ketamine has a profound impact on the response to endotoxic shock. This review summarizes our findings on the mechanisms of action by which ketamine is able to modulate the nitric oxide, cyclo-oxygenase and heme-oxygenase enzyme systems to attenuate endotoxin-induced organ dysfunction.

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“…O LPS, em ratos, determina diminuição da pressão arterial e do fl uxo sangüíneo mesentérico, fenômenos atenuados pelo pré-tratamento com L-NAME (2,14) . Contudo, foi constatado que há também, com a administração do L-NAME, diminuição do fl uxo sangüíneo capilar na mucosa do sistema digestório, aumentado pela administração de LPS (4,15,17) . Assim, é possível admitir que, nas condições experimentais a que os animais foram submetidos no presente estudo, haja comprometimento da microcirculação das camadas musculares do sistema digestório.…”

Section: Discussionunclassified

Efeito do lipopolissacarídio bacteriano sobre o esvaziamento gástrico de ratos: avaliação do pré-tratamento com Nw-nitro-L-arginine methyl ester (L-NAME)

Collares

Vinagre

2006

Arq. Gastroenterol.

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ARQGA/1240 INTRODUÇÃO O esvaziamento gástrico (EG) é um processo complexo de transferência ordenada do conteúdo gástrico para o intestino delgado, resultante da ação de mecanismos estimuladores e inibitórios que controlam a atividade motora do estômago, piloro e duodeno (16) .O lipopolissacarídio (LPS) bacteriano, por via intravenosa, determina retardo do EG de uma refeição líquida em ratos. Este fenômeno guarda relação com a dose da endotoxina, ocorre precocemente e há evidências da participação do nervo vago no mesmo (9) . Foi também observado que o pré-tratamento com o próprio LPS aboliu este efeito, reproduzindo o fenômeno de tolerância precoce, já descrito para outras alterações produzidas pela endotoxina (10) . Mais recentemente, foi verifi cado, in vivo, que o pré-tratamento intravenoso (iv) com azul de metileno ou com a dexametasona bloqueou o retardo do EG precoce e tardio, respectivamente, determinado pela toxina (11) . Estas observações sugerem a participação do óxido nítrico (ON) no fenômeno, visto que o azul de metileno EFEITO DO LIPOPOLISSACARÍDIO BACTERIANO SOBRE O ESVAZIAMENTO GÁSTRICO DE RATOS: avaliação do pré-tratamento com N W -nitro-L-arginine methyl ester (L-NAME)Edgard Ferro COLLARES 1 e Adriana Mendes VINAGRE 2 RESUMO -Racional -Há evidências de que o óxido nítrico participa do mecanismo de retardo do esvaziamento gástrico determinado pelo lipopolissacarídio bacteriano. Objetivo -Avaliar o efeito do pré-tratamento com N w -nitro-L-arginine methyl ester, um inibidor competitivo das óxido nítrico-sintetases, sobre o fenômeno. Material e métodos -Utilizaram-se ratos, Wistar, machos, SPF ("specifi c-pathogen free"), adultos, adaptados às condições do laboratório, que após 24 horas de jejum alimentar foram pré-tratados endovenosamente com veículo (salina) ou N w -nitro-L-arginine methyl ester nas doses de 0,5, 1, 2,5 e 5 mg/kg. No tratamento, administrou-se endovenosamente veículo (salina) ou lipopolissacarídio (50 µg/kg). O intervalo entre o pré-tratamento e o tratamento foi de 10 minutos, e entre este e a avaliação do esvaziamento gástrico foi de 60 minutos. O esvaziamento gástrico foi avaliado indiretamente através da determinação da retenção gástrica da solução salina marcada com fenol vermelho 10 minutos após administração por via orogástrica. Resultados -Entre os animais pré-tratados com veículo, o tratamento com lipopolissacarídio determinou elevação signifi cativa da retenção gástrica (média = 57%) em relação aos tratados com veículo (38,1%). O pré-tratamento com as diferentes doses de N w -nitro-L-arginine methyl ester não modifi cou a retenção gástrica nos animais controles do tratamento. O pré-tratamento com N w -nitro-L-arginine methyl ester com a dose de 1 mg/kg determinou redução discreta, mas signifi cativa, na retenção gástrica (52%) nos animais tratados com lipopolissacarídio, em relação ao observado naqueles com pré-tratamento e tratamento com veículo (35,9%). Nos animais pré-tratados com 2,5 e 5 mg/kg de N w -nitro-L-arginine methyl ester e tratados com lipopolissacarídio...

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Gastric nitric oxide synthase expression during endotoxemia: Implications in mucosal defense in rats

Cited by 41 publications

References 32 publications

Rapid Up-Regulation of Endothelial Nitric-Oxide Synthase in a Mouse Model ofEscherichia coliLipopolysaccharide-Induced Bladder Inflammation

Rapid Up-Regulation of Endothelial Nitric-Oxide Synthase in a Mouse Model ofEscherichia coliLipopolysaccharide-Induced Bladder Inflammation

The Gut in Systemic Inflammatory Response Syndrome and Sepsis

Efeito do lipopolissacarídio bacteriano sobre o esvaziamento gástrico de ratos: avaliação do pré-tratamento com Nw-nitro-L-arginine methyl ester (L-NAME)

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