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BACKGROUND & AIMS Cigarette smoking has been associated with peptic ulceration. However, the ulcerogenic mechanisms are still undefined. The aim of this study was to investigate the effects and possible mechanisms of cigarette smoke on ethanol- or cold-restraint stress-induced gastric damage. METHODS Rats were exposed to cigarette smoke followed by either(More)
Cigarette smoking is associated with gastric mucosal damage in humans. For this study, a smoke chamber was designed to investigate the effects of passive smoking on gastric ulceration. Different concentrations of cigarette smoke (0%, 1%, 2%, and 4%) were perfused into a chamber for one hr in which conscious rats were placed. This one-hr smoke exposure(More)
Epidemiologic studies have shown that cigarette smoking is closely related to peptic ulcer disease. The mechanisms by which cigarette smoking adversely affects gastric mucosa have been suggested and elucidated. This article reviews some of the mechanisms involved in cigarette smoking-related gastric ulceration and healing. Experimental findings suggest that(More)
Since little is known about the role of P2Y receptors (purinoceptors) in duodenal mucosal bicarbonate secretion (DMBS), we sought to investigate the expression and function of these receptors in duodenal epithelium. Expression of P2Y(2) receptors was detected by RT-PCR in mouse duodenal epithelium and SCBN cells, a duodenal epithelial cell line. UTP, a(More)
BACKGROUND Cigarette smoking was shown to delay gastric ulcer healing and reduce synthesis of mucus, which is important for gastric ulcer protection and healing. Polyamines are important in these processes. AIMS To study the effects of cigarette smoking on the synthesis of mucus and to investigate if such an effect is acting by interference with the(More)
Epidemiological studies have shown that cigarette smoking is associated with peptic ulceration. This study aims to investigate the mechanisms by which cigarette smoking delays ulcer healing in rats. Gastric ulcers were induced by applying acetic acid to the luminal surfaces in rats. Twenty-four hours later, rats were exposed to different concentrations of(More)
Accumulating evidence indicates that capsaicin sensitive afferent fibers play a pivotal role not only in gastroprotection but also in ulcer healing. Denervation of capsaicin sensitive afferent fibers exerts an adverse action on these effects. However, whether such an action is mediated through a depression on epidermal growth factor (EGF) is undefined. In(More)
The roles of neutrophil aggregation, inducible nitric oxide synthase activation and chemoattractant, leukotriene B4, in potentiation of the cigarette smoke effect on ethanol-induced gastric mucosal damage were studied. Smoke exposure markedly increased gastric lesion formation following ethanol administration and this was accompanied by substantial increase(More)
Cigarette smoking is associated with peptic ulcer diseases. Smokers have lower levels of salivary epidermal growth factor (EGF) than nonsmokers. We investigated whether reduction of EGF is involved in the delay of gastric ulcer healing by cigarette smoking. Rats with acetic acid-induced ulcers were exposed to cigarette smoke (0, 2, or 4% vol/vol) 1 day(More)
Because human duodenal mucosal bicarbonate secretion (DMBS) protects duodenum against acid-peptic injury, we hypothesize that estrogen stimulates DMBS, thereby attributing to the clinically observed lower incidence of duodenal ulcer in premenopausal women than the age-matched men. We found that basal and acid-stimulated DMBS responses were 1.5 and 2.4-fold(More)