| 1. |
|
|
| 2. |
- Bove, Mogens, 1949, et al.
(author)
-
Acid challenge to the esophageal mucosa: effects on local nitric oxide formation and its relation to epithelial functions
- 2005
-
In: Dig Dis Sci. - : Springer Science and Business Media LLC. - 0163-2116 .- 1573-2568. ; 50:4, s. 640-8
-
Journal article (peer-reviewed)abstract
- To evaluate the effect of esophageal acid exposure on epithelial function, transmucosal potential, histopathological markers of acute tissue damage, and local nitric oxide production were examined in healthy volunteers treated with proton pump inhibitors (group I), patients with treated reflux disease (group II), and patients with untreated erosive reflux disease (group III). The participants were randomized to esophageal perfusion with either saline or HCl. Denominators of acute acid exposure were balloon cells in superficial layers and superficial densification. The nitric oxide concentrations in groups I to III increased from < 1, 10.0+/-10.0, and 20.6+/-19.9 ppb, respectively, to 300+/-80, 1360+/-1080, and 920+/-700 ppb after HCl infusion (P < 0.001). Inducible nitric oxide synthase was consistently expressed in the epithelium. Blood flow was lower among reflux patients but did not correlate with acid exposure or nitric oxide. Nitric oxide is formed following acid perfusion and predominantly in gastroesophageal reflux disease.
|
|
| 3. |
- Bove, Mogens, 1949, et al.
(author)
-
Acid challenge to the human esophageal mucosa: effects on epithelial architecture in health and disease
- 2005
-
In: Dig Dis Sci. - : Springer Science and Business Media LLC. - 0163-2116 .- 1573-2568. ; 50:8, s. 1488-96
-
Journal article (peer-reviewed)abstract
- The histological changes that occur in the squamous epithelium in response to acute acid challenge was examined in healthy controls and proton pump inhibitor-treated gastroesophageal reflux disease (GERD) patients and related to the state of untreated erosive GERD in a saline-controlled, randomized perfusion study. In the basal state a stepwise significant increase in the thickness of the basal cell layer, papillary length, and dilatation of intercellular spaces (DIS) was seen when the three groups were compared. Acid perfusion induced a slight increase in the height of the basal cell layer mainly in healthy volunteers; this layer appears to be reactive to acute acid challenge as well as to acid suppressive therapy. DIS increases promptly in response to acute acid exposure in the healthy epithelium but no changes were seen in the lengths of the papillae or regarding DIS in the GERD patients. A protective effect of luminal nitric oxide on DIS development is suggested.
|
|
| 4. |
- Bove, Mogens, 1949, et al.
(author)
-
Epithelial barrier integrity and intraluminal nitric oxide production in response to acid perfusion of the ferret oesophagus
- 2005
-
In: Acta Physiol Scand. - 0001-6772. ; 183:2, s. 211-8
-
Journal article (peer-reviewed)abstract
- AIM: To evaluate the source and role of acid-induced intraluminal nitric oxide (NO) production in the oesophagus by studying how the exposure of the oesophagus to acid affects NO release, via the NO-producing enzyme NO synthase and its relation to changes in epithelial barrier integrity. METHODS: Ferrets were anaesthetized and their oesophagi were divided at both ends. The test subjects were pre-treated with the intravenous NO synthase inhibitors N(G)-nitro-L-arginine-methyl ester (L-NAME, 100 mg kg(-1)) and 1400W (12 mg kg(-1)). Untreated and N(G)-nitro-D-arginine-methyl ester pre-treated (D-NAME, 100 mg kg(-1)) animals served as controls. The oesophagus was then perfused with either HCl (0.1 m) or physiological saline for 20 min. The intraluminal NO concentration was determined before and after the acid/saline infusion while the transmucosal potential difference (PD) was monitored continuously. Oesophageal biopsies were examined for expression of inducible NO synthase using immunohistochemistry. RESULTS: The intraluminal NO concentration increased after acid exposure. This was blocked by L-NAME and 1400W, but not by D-NAME. The peak PD response was not affected by agents affecting NO synthesis, while the plateau response was attenuated by L-NAME, D-NAME and 1400W. Immunohistochemistry revealed inducible NO synthase expression in the epithelium. CONCLUSIONS: Exposing the ferret oesophageal mucosa to acid elicited an increase in juxtamucosal NO formation through the activation of inducible NO synthase. The corresponding electrophysiological observations suggested an association between mucosal NO production and epithelial integrity.
|
|
