Ablation of primary afferent neurons by neonatal capsaicin treatment reduces the susceptibility of the portal hypertensive gastric mucosa to ethanol-induced injury in cirrhotic rats

Câmara, Paula Rs; Ferraz, Gerson J. N.; Franco‐Penteado, Carla F.; Sbragia-Neto, Lourenço; Meirelles, Luciana Rodrigues de; Teixeira, Simone Aparecida; Muscará, Marcelo N.; Velloso, Lı́cio A.; Antunes, Edson; Ferraz, José G.

doi:10.1016/j.ejphar.2008.05.004

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…Studies have shown different results under the two models of portal hypertensive gastropathy: in the BDL model there is evidence of alterations of basal hemodynamic parameters which augment the gastric lesions [17,19,44] ; these lesions were reduced in the PVS model. The low damage resistance in the BDL group could be due to the fact that, at the same time, the liver is involved and the pentobarbital anesthesia was used.…”

Section: Discussionmentioning

confidence: 99%

“…BDL rats) treated under KX anesthesia had less gastric mucosal damage from ethanol stimulus. While the specific process by which KX anesthetics affect GBF is unknown, previous studies demonstrate that glucose levels are improved under treatment with KX anesthetics via α2-adrenoreceptor activation [19] and in turn the glucose acts to impair vagal activity in the stomach [20] . Therefore, it suggests that the increase of glucose serves to increase the pressure of GBF.…”

Section: Discussionmentioning

confidence: 99%

“…Basal GBF was then recorded for 5 min and experiments performed according to the protocol described previously [17] . GBF was recorded throughout the 60 min and maximum changes in flow were expressed as percentage change over basal [19] .…”

Section: Ethanol-induced Gastric Damagementioning

confidence: 99%

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Effect of anesthetics on gastric damage using two models of portal hypertension

Câmara

Moi²,

Ferraz³

et al. 2010

WJGPT

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AIM:To investigate the effect of sodium pentobarbitone (SP) or ketamine/xylazine (KX) anesthetics on acute gastric injury. METHODS:Portal hypertension was induced by bile duct ligation (BDL) or portal vein stenosis (PVS). Ethanol (EtOH)-induced gastric damage was assessed using ex vivo gastric chamber experiments. Gastric blood flow (GBF) was also measured by laser doppler flowmetry. RESULTS:EtOH-induced gastric damage was reduced in BDL rats under KX anesthesia in comparison to those under SP anesthesia. GBF dysfunction in fasted BDL rats was partially restored under KX anesthesia. In contrast, in fasted PVS rats, EtOH-induced gastric damage was increased under KX anesthesia while GBF was reduced. CONCLUSION:The use of KX anesthesia in experimental procedures involving cirrhotic rats (but not those with pure portal hypertension) is preferable to SP anesthesia. Câmara PRS, Moi GP, Ferraz JGP, Zeitune JMR. Effect of anes thetics on gastric damage using two models of portal hyperten sion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of anesthetics on gastric damage using two models of portal hypertension

Câmara

Moi²,

Ferraz³

et al. 2010

WJGPT

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“…Human studies have shown increased, decreased, or unchanged levels of PGs in the gastric mucosa, whereas animal models of PHT gastropathy generally show a reduction of PGs [9][10][11][12]. Uniformly, however, a reduction in PGs by inhibitors causes increased gastric mucosal damage in both animal models and patients with PHT [11,13,14]. The primary enzyme responsible for PG synthesis, cyclooxygenase (COX), exists in at least three isozymes.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of cyclooxygenase-1 is involved in gastric mucosal apoptosis via death signaling in portal hypertensive rats

Zeng

Ying

et al. 2009

Cell Res

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Portal hypertension (PHT) gastropathy is a frequent complication of liver cirrhosis and one of the leading causes of death from cirrhosis. Apoptosis is widely considered to be an active energy-dependent mode of cell death and a distinct entity from necrotic cell death. It is unclear whether gastric mucosal apoptosis is involved in PHT gastropathy. Prostaglandins (PGs) produced through cyclooxygenase (COX) are thought to play a key role in protection of the gastrointestinal mucosa from injury and apoptosis. However, the role of COX in PHT gastropathy is still not clearly understood. The aims of this study were to investigate whether (1) gastric mucosal apoptosis is involved in PHT gastropathy and (2) downregulation of COX contributes to this apoptosis. In this study, we show that gastric mucosal apoptosis was remarkably increased while mucosal proliferation was inhibited in PHT rats. Gastric mucosal COX-1 was significantly suppressed at both the mRNA and protein levels, and PGE 2 was reduced in PHT rats. Further, PGE 2 treatment suppressed gastric mucosal apoptosis in PHT rats. However, gastric mucosal COX-2 levels did not differ between sham-operated rats and PHT rats. Gastric mucosal levels of tumor necrosis factor-α (TNF-α) and Fas ligand, but not TNF-related apoptosis-inducing ligand, were increased, and activated caspase-8 and caspase-3 levels were upregulated in PHT rats. The release of cytochrome c from the mitochondria to the cytosol was not observed in PHT rats. Our data indicate that downregulation of COX-1 is involved in gastric mucosal apoptosis via death signaling-mediated type-I cell death in PHT rats.

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