Prevention of the rehaemorrhage of bleeding peptic ulcers: effects of Helicobacter pylori eradication and acid suppression.

AIM: This study aimed to investigate the consequences of Helicobacter pylori eradication and acid suppression on rehaemorrhage caused by bleeding peptic ulcers. METHODS: A total of 320 patients who had been diagnosed with bleeding peptic ulcers between January 1994 and December 2001 were included in the study. Cases between 1994 and 1997, prior to the introduction of eradication therapy, were assigned to group A, whereas those between 1998 and 2001, after the eradication therapy, were assigned to group B. RESULTS: Of the 320 cases, 162 were designated as group A (113 gastric ulcers and 49 duodenal ulcers) and 158 as group B (116 and 42, respectively). Rehaemorrhage occurred in 24 cases (15%) and five cases (3%) in groups A and B, respectively, presenting a significantly decreased rate of rehaemorrhage in group B. Among those without eradication, rehaemorrhage was observed in 15 of 128 cases (12%) that received treatment with histamine(2)-receptor antagonist (famotidine), and 14 of 142 cases (10%) treated with proton-pump inhibitors, with no significant difference between the two. CONCLUSIONS: Helicobacter pylori eradication lowered the rates of rehaemorrhage. Treatment with histamine(2)-receptor antagonist or proton-pump inhibitors did not produce a difference in the rate of rehaemorrhage.

Effects of antioxidative agents on apoptosis induced by ischaemia-reperfusion in rat intestinal mucosa.

BACKGROUND AND AIM: We have previously demonstrated that ischaemia-reperfusion induces apoptosis in the intestinal mucosa. To evaluate that reactive oxygen species enhanced intestinal apoptosis after ischaemia-reperfusion, we examined whether antioxidants reduced apoptosis. METHODS: Rats were infused through a duodenal tube with antioxidative agents, glutathione, rebamipide and dymethylsulfoxide during 2 h before an ischaemic insult. The superior mesenteric artery was occluded for 60 min, followed by 60 min reperfusion. Apoptosis was evaluated by percentage fragmented DNA (fragmented DNA/total DNA) and immunochemical staining. RESULTS: Increase in apoptosis in the intestinal mucosa after ischaemia-reperfusion was attenuated by intraduodenal infusion of antioxidative agents, but was not completely abolished. CONCLUSION: Scavenging effects of the antioxidative agents attenuated increases in intestinal apoptosis, indicating that oxidative stress after ischaemia-reperfusion plays an important role in induction of apoptosis in the intestinal mucosa.

Apoptosis induced by ischemia-reperfusion and fasting in gastric mucosa compared to small intestinal mucosa in rats.

The effect of ischemia-reperfusion and 48-hr fasting on apoptosis was characterized in rat gastric mucosa and compared to small intestinal mucosa. Under halothane anesthesia, the celiac artery or superior mesenteric artery in the rat was occluded for 60 min followed by reperfusion. Occlusion of the celiac artery reduced blood flow in the stomach and occlusion of the mesenteric artery reduced blood flow in the small intestine. Additional rats were fasted for 48 hr to evaluate the effect of fasting on mucosal apoptosis. The ratios of fragmented DNA to total DNA, electrophoresis, and immunohistochemical staining were examined after ischemia-reperfusion or fasting. Apoptosis was not induced significantly in the gastric mucosa after ischemia-reperfusion, although it increased dramatically in the intestinal mucosa after ischemia-reperfusion. Further, after 48 fasting, apoptosis was induced in the small intestine, but not in the stomach. These results indicate that rat gastric mucosa is not as sensitive as small intestinal mucosa to ischemia-reperfusion or fasting-induced apoptosis.

An air-liquid interface promotes the differentiation of gastric surface mucous cells (GSM06) in culture.

The gastric surface epithelium is situated at an air-liquid interface because the luminal surface of the alimentary tract is in continuity with the air phase. However, the effects of this microenvironment on the gastric epithelium remain unclear. The aim of this study was to clarify the effects of an air-liquid interface on gastric epithelial cell biology. Gastric surface mucous cells (GSM06) were cultured at an air-liquid interface. Cultured cells were examined by histology, histochemistry, and transmission electron microscopy. When the cells were cultured at an air-liquid interface, the surface cells on the collagen gel became tall columnar and secreted periodic acid-Shiff-positive substances at the apical surface. These cells indicated many mucous granules in the apical cytoplasm and organized the basal lamina at the contact side with the gel. In contrast, under immersed condition, the surface cells showed immature features. This is the first report of an air-liquid interface promoting the differentiation of gastric surface mucous cells in a reconstruction culture of the gastric surface epithelial layer, suggesting that an air-liquid interface may function as a crucial luminal factor to maintain the homeostasis of gastric mucosa.

Histaminergic control of mucosal repair in the small intestine.

The aim of the present paper was to summarize histamine-mediated repair of rat intestinal mucosa. To evaluate intestinal repair, we examined lipid transport (an index of intestinal mucosal function) after 15 minutes occlusion of the superior mesenteric artery. Rats were pretreated with alpha-fluoromethylhistidine (a suicide inhibitor of histidine decarboxylase, a synthesizing enzyme of histamine), H1-receptor antagonist (chlorpheniramine maleate), H2-antagonist (cimetidine), or H3-antagonist (thioperamide) before ischemia-reperfusion (I/R). Lipid transport to rat mesenteric lymph decreased significantly 24 hours after I/R in all groups tested compared to sham-treated rats. Lipid transport was restored 48 hours after I/R in the vehicle-pretreated control group. Lipid transport was not restored to the control level 48 hours after I/R in rats pretreated with H1-antagonist and a suicide inhibitor of histidine decarboxylase. In contrast, intestinal function was restored to the control level 48 hours after I/R in rats pretreated with H2- and H3-antagonists. These results support our previous findings that newly formed histamine after I/R plays an important role in mucosal recovery through H1-receptors.