An <i>in vivo</i> model for gastric physiological and pathophysiological studies in the mouse

Henriksnäs, Johanna; Phillipson, Mia; Petersson, Joel; Engstrand, Lars; Holm, Lena

doi:10.1111/j.1365-201x.2005.01434.x

Cited by 12 publications

(13 citation statements)

References 34 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A relevant question is whether the acid-base values in Ringer solution-treated mice are to be considered abnormal, i.e., acidemic, or not. Typical values for pH and PCO 2 previously reported in isoflurane-anesthetized spontaneously breathing mice have ranged, respectively, from 7.35 and 39 mmHg (27) to 7.25 and 49 mmHg (8). These values are in fair agreement with those in the Ringer solutioninfused mice found here.…”

Section: Discussionsupporting

confidence: 81%

See 1 more Smart Citation

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice

Sjöblom

Nylander²

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Sjöblom M, Nylander O. Isoflurane-induced acidosis depresses basal and PGE 2-stimulated duodenal bicarbonate secretion in mice. Am J Physiol Gastrointest Liver Physiol 292: G899 -G904, 2007. First published December 7, 2006; doi:10.1152/ajpgi.00398.2006.-When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE 2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na 2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE 2 was used to stimulate DMBS. In Ringer solution-infused mice, isofluraneinduced acidosis became worse with time. The blood pH was 7.15-7.21 and the base excess was about Ϫ8 mM at the end of experiments. The continuous infusion of Na 2CO3 solution completely compensated for the acidosis. The blood pH was 7.36 -7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE 2-stimulated DMBS were markedly greater in animals treated with Na 2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na 2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE 2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.anesthesia; murine physiology; in vivo; duodenal mucosal protection

show abstract

Section: Discussionsupporting

confidence: 81%

“…However, this anesthetic is not without side effects. A commonly reported side effect of isoflurane anesthesia in mice is disturbance of the acid-base balance, e.g., acidosis (8,13,24,31).…”

mentioning

confidence: 99%

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice

Sjöblom

Nylander²

2007

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

show abstract

“…We have previously shown in a rat model (3) and in this mouse model (16) that the mucus layer can be divided into two layers: one that can be removed (designated loosely adherent) and one that cannot be removed by mechanical means without destroying the epithelial layer (the firmly adherent layer). From another study, we (28) have also concluded that it is the firmly adherent layer that is important for the protection against luminal acid, because it is in this layer that the pH gradient is formed.…”

Section: Discussionmentioning

confidence: 99%

“…Blood flow was measured with laser-Doppler flowmetry equipment (Periflux instruments Pf3 and Pf4001, Perimed; Stockholm, Sweden), which has previously been used to study microcirculatory blood flow of the gastric mucosa in the mouse model (16). The laser probe was held in a fixed position in the chamber solution at a distance of 1-2 mm above the mucosa by a micromanipulator.…”

Section: Blood Flow Measurementsmentioning

confidence: 99%

See 1 more Smart Citation

Impaired mucus-bicarbonate barrier inHelicobacter pylori-infected mice

Henriksnäs

Phillipson²,

Storm³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

To resist the harsh intrinsic milieu, several lines of defense exist in the stomach. The aim of this study was to investigate the effect of the gastric pathogen Helicobacter pylori on these mechanisms in vivo. We used FVB/N mice expressing human ␣-1,3/4-fucosyl transferase (producing Lewis b epitopes) and inoculated with H. pylori 1. Mice were anesthetized with isoflurane or Hypnorm-midazolam, the stomach was exteriorized, and the surface of the corpus mucosa was exposed. Mucus thickness was measured with micropipettes, juxtamucosal pH (pHjm) was measured with pH-sensitive microelectrodes, blood flow was measured with laser-Doppler flowmetry, and mRNA levels of the bicarbonate transporter SLC26A9 were quantified with real-time PCR. The increase in mucosal blood flow seen in response to luminal acid (pH 1.5) in control animals (140 Ϯ 9% of control) was abolished in infected mice. The firmly adherent mucus layer was significantly thinner in infected mice (31 Ϯ 2 m) than in control mice (46 Ϯ 5 m), and no mucus accumulation occurred in infected mice. pHjm decreased significantly more on exposure to luminal acid in infected mice (luminal pH 1.5, pH jm 2.4 Ϯ 0.7) than in control mice (pHjm 6.4 Ϯ 0.5). Despite reduced pHjm, SLC26A9 mRNA expression was significantly, by increased 1.9-fold, in infected mice. The reduction in pH jm by infection with H. pylori might be due to a reduced firmly adherent mucus layer, increased mucus permeability to H ϩ , and/or inhibition of bicarbonate transport. The upregulation of SLC26A9 in H. pylori-infected epithelium might be a result of continuous inhibition of the transporter, e.g., by ammonium, a H. pylori product, which has been previously shown to inhibit SLC26A9. juxtamucosal pH; blood flow; laser-Doppler flowmetry; permeability

show abstract

Assessment of Mucus Thickness and Production In Situ

Holm

Phillipson

2011

Methods in Molecular Biology

View full text Add to dashboard Cite

The nature of the mucus gel layer covering the gastrointestinal tract makes it difficult to study outside its natural site attached to the mucosa. Here, we describe a technique for intravital microscopy studies of the mucus gel layer from the stomach down to the colon in anesthetized rats and mice. Mucus thickness and accumulation rate in each segment of the gastrointestinal tract is measured with a micropipette technique under observation through a stereomicroscope. In this way, the nature of the mucus gel in vivo is readily studied, and effects of interventions or disease on the mucus can be determined in longitudinal studies or by comparing animals. Using this technique, we have been able to demonstrate that there are two forms of mucus gel adherent to the stomach and colon mucosa: one layer which is removable by suction and an underlying firm adherent gel layer, while in the small intestine, all mucus adhering to the mucosa can easily be removed.

show abstract

An in vivo model for gastric physiological and pathophysiological studies in the mouse

Abstract: This model has great potential for investigations of gastrointestinal physiology and pathophysiology and can be applied for Helicobacter pylori infection studies.

Cited by 12 publications

References 34 publications

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice

Impaired mucus-bicarbonate barrier inHelicobacter pylori-infected mice

Assessment of Mucus Thickness and Production In Situ

Contact Info

Product

Resources

About

An in vivo model for gastric physiological and pathophysiological studies in the mouse

Abstract: This model has great potential for investigations of gastrointestinal physiology and pathophysiology and can be applied for Helicobacter pylori infection studies.

Cited by 12 publications

References 34 publications

Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

Isoflurane-induced acidosis depresses basal and PGE2-stimulated duodenal bicarbonate secretion in mice

Impaired mucus-bicarbonate barrier inHelicobacter pylori-infected mice

Assessment of Mucus Thickness and Production In Situ

Contact Info

Product

Resources

About

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice

Isoflurane-induced acidosis depresses basal and PGE₂-stimulated duodenal bicarbonate secretion in mice