Gastric hypersecretion associated to iodoacetamide-induced mild gastritis in mice

Abstract

Disturbances of gastric motor, secretory and/or sensory functions are frequently associated with gastritis. The aim of this study was to characterize motor and secretory alterations associated to chemically-induced gastritis in mice. Mild gastritis was induced with 0.1% iodoacetamide administered intragastrically and added to the drinking water for a 6 days period. A significant loss of body weight and a reduction in food and water intake was observed in iodoacetamide-treated animals compared with those receiving vehicle. At the end of the treatment period, no macroscopic alterations were observed in the gastric mucosa of iodoacetamide-treated mice. However, histological sections revealed a mixed inflammatory infiltrate, with a predominance of mast cells in the submucosa; suggesting a mild gastritis. Gastric emptying rate of a nutrient solid meal was not modified in mice with gastritis compared with normal controls. In animals with gastritis, basal gastric acid secretion was increased compared with normal controls. Basal gastric acid secretion was not modified by either indomethacin or compound 48/80. Secretory response to secretagogues (pentagastrin and histamine) was enhanced during gastritis. Hypersecretory responses to both gastrin and histamine in iodoacetamide-treated mice were blocked by the mast cell stabilizer sodium cromoglycate, and enhanced by indomethacin, without affecting the secretory response in normal mice. These results suggest that mild gastritis alters gastric acid secretory responses through a mechanism related, at least partially, to mast cells activation. Moreover, prostaglandins also modulate secretory responses during mild inflammation. This animal model of gastritis might be useful to characterize pathophysiological changes and potential therapeutic targets in secretory-related gastric pathologies.

Role of endogenous nitric oxide in mucosal defense of inflamed rat stomach following iodoacetamide treatment

“…The present study further showed that NO produced by iNOS also acts negatively on acid secretion in the inflamed stomach, i.e., under subchronic damage, in addition to cNOS/ NO. By contrast, Piqueras et al (2003) reported that basal acid secretion increased in animals treated with iodoacetamide and this response was associated with mast cell activation, the results being in marked contrast with those obtained in the same gastritis model in the present study. At present, these discrepancies remain unexplained, but may be due to different experimental conditions, such as the degree of inflammation.…”

Experimental gastritis leads to anxiety- and depression-like behaviors in female but not male rats

“…In the present study we observed that the gastric inflammation was successfully induced by IAA treatment in rats of either gender, as assessed by increased MPO activities in IAA-treated rats. A potential drawback of IAA-induced gastritis model is the significant reduction of water intake [36,37]. Nonetheless, previous reported analysis of the circadian activity patterns revealed that IAA reduced drinking, feeding and locomotor activity only during the dark phase to a significant extent, suggesting that the reduction of water intake is not primarily taste-related but, together with the decrease in feeding and locomotor activity, reflects a behavioral consequence of gastritis [22].…”

Somatostatin Receptor type 2 Mediates Bombesin‐Induced Inhibition of Gastric Acid Secretion in Mice

“…Doses of compounds were selected according to previous studies in mice (Martínez et al . 1998; Piqueras et al . 2003).…”

“…Gastric acid secretion was monitored in urethane‐anaesthetized mice as previously described, with minor modifications (Martínez et al . 1998; Piqueras et al . 2003).…”