Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indirect pieces of evidences indicate the correlation between insulin level and pathogenesis of peptic ulcer. In the present study, serum insulin releasing level after glucose loading was determined in 16 patients with duodenal ulcer (DU) using radioimmunoassay, and was compared with that of normal controls. The peak insulin level (PIL) in DU patients was significantly higher than that of normal individuals (P less than 0.05), the measurements of gastric acidity, insulin level and the gastroscopic examination were carried out both before and after the treatment. The rebound phenomenon of gastric acidity (BAO) was correlated to that of PIL (r = 0.85). The possible relationship between insulin level and DU was discussed.
Zhonghua Nei Ke Za Zhi 1989 Sep
PMID:[Duodenal ulcer and the insulin releasing level]. 269 26

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.
Zhonghua Nei Ke Za Zhi 1989 Feb
PMID:[Clinical characteristics of bile reflux gastritis]. 273 41

OBJECTIVE To explore the changes of rat gastric mucosal barrier under conditions of water immersion restraint stress. METHODS Eighty rats were randomly divided into Group A (20 rats), B (40 rats) and C (20 rats) after being fasted for 24 hours. And then Group A was divided into two subgroups with ten rats in each. The two subgroups in Group A were given normal saline or omeprazole respectively while under the stress condition. The changes of gastric acid or bicarbonate secretion were determined. Group B (40 rats) were randomly divided into four subgroups,which were subgroup control, 1h, 2h and 4h after beginning of the stress. The quantity of glandular mucosal adherent mucus, the thickness of mucus gel layer and ulcer index were measured after stress in Group B. The glandular mucosal samples were labeled by Lanthanum and observed by transmission electromicroscopy. Group C was randomly divided into two subgroups in the same way with Group A. And each subgroup received normal saline or omeprazole respectively H(+) loss in gastric lumen was calculated by determining the difference of acidity between lavage and drainage fluid H(+) concentration. RESULTS It was found that gastric alkaline secretion decreased progressively (P < 0.05), while gastric acid secretion increased progressively under stress conditions (P < 0.05). The mucus quantity(A/g) in the four subgroups in Group B were 0.137 +/- 0.030, 0.143 +/- 0.012, 0.066 +/- 0.016 and 0.016 +/- 0.016 respectively. The mucus gel thickness(microm) were 71.08 +/- 5.85, 74.50 +/- 12.85, 57.63 +/- 6.45 and 51.35 +/- 2.84 respectively. The ulcer index were 0.2 +/- 0.1,0.4 +/- 0.1,5.2 +/- 1.3 and 10.0 +/- 0.5 respectively. Statistics showed that the mucus quantity was correlated with the mucus gel thickness positively(r = 0.89), while either of them was correlated with the ulcer index negatively(r = 0.85 and "r = 0.83). And it was also found that Lanthanum rarely stained the glandular mucosa in control subgroup, while heavily in stress subgroups. In the subgroup receiving normal saline in Group C, within 5 hours after the beginning of stress, the amount of H(+) loss per hour(micromol) was 2.03 +/- 0.12, 2.00 +/- 0.20, 1.93 +/- 0.49, 2.70 +/- 0.44 and 3.37 +/- 0.35 respectively. It was demonstrated that the amount of H(+) loss was stable within 2h after stress, then increased obviously in normal saline subgroup significantly (P < 0.01). In omeprazole subgroup, the amount of H(+) loss (micromol) was 7.46 +/- 1.22, 4.56 +/- 0.35, 3.11 +/- 0.81, 2.32 +/- 1.42 and 2.13 +/- 1.60, which decreased progressively, however still higher than those in normal saline subgroup (P "< 0.01). CONCLUSIONS The results suggest that gastric bicarbonate secretion is inhibited; gastric barrier is damaged; and hydrogen permeability through gastric mucosal barrier increases under stress conditions.
Zhonghua Nei Ke Za Zhi 2002 Jun
PMID:[Changes of rat gastric mucosal barrier under stress conditions]. 1213 97