摘要:

AbstractAt Royal Perth Hospital, Western Australia in April 1982, spiral bacteria were first cultured from a gastric biopsy specimen. Several important taxonomic features were identified which indicated that these bacteria represented a new genus. In October 1989 the new genus nameHelicobacterwas published.Helicobacter pyloriovercomes gastric defence mechanisms by means of its powerful urease enzyme, by its spiral shape allowing it to penetrate mucus, by adherence to the gastric mucosa and by various mechanisms which enable it to evade the immune response.

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01292.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractPeptic ulcer disease is twice as common in people living in South China when compared with those in North China. However, the gastric cancer rate in North China is three times that of South China. The overallHelicobacter pyloriprevalence rate is similar in North and South China populations and it is higher than Caucasians living in Western societies. However, there is a significantly higher prevalence ofH. pyloriseropositivity among those who live in the high gastric cancer areas of China. On the other hand, there is no significant difference in theH. pyloripositive rate in the peptic ulcer disease patients between the two regions of China. Other permissive/associated co‐factors in the development of peptic ulcer disease or gastric cancer remain unknown at this stag

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01293.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractHelicobacter pyloriinfection is the most common cause of duodenal ulcer disease, yet duodenal ulcer is an uncommon outcome ofH. pyloriinfection. We reviewed the possible explanations such as differences in the host or in the strain ofH. pylori.Host factors reviewed included genetic susceptibility toH. pyloriinfection and excess gastric acid secretion. The role of potentialH. pylorivirulence factors not present in all strains such as thecagAgene and the results of other molecular methods to identify disease‐specific differences among isolates was also reviewed. Although cure ofH. pyloriinfection resolves gastrin releasing peptide stimulated acid secretion there was no change in parietal cell mass. Twin studies have shown genetic differences inH. pylorisusceptibility. There was no difference in the prevalence of thecagAgene betweenH. pyloriinfected asymptomatic volunteers and duodenal ulcer patients (P= 1.0). DNA‐DNA hybridization of whole genomic DNA in solution and cluster analysis of rep‐PCR genomic DNA fingerprints suggest that isolates from patients with duodenal ulcer disease are different from those obtained from individuals with asymptomatic gastritis. Cluster analysis of the rep‐PCR DNA fingerprints revealed two major groups of the strains; one set consisted of strains from patients with duodenal ulcer disease and the second cluster consisted largely of strains from individuals with asymptomatic gastritis. Recent molecular studies suggest that disease‐specific cell lineages or strains may exist amongH. pyloriisolates leading to the various outcomes observed in patients withH. pylori

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01294.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractInfection with the bacteriumHelicobacter pyloriis associated with both the development of gastritis and an attenuation in the hydrophobic properties of the stomach. In order to better understand the effect of ammonium, one of the major products ofH. pyloriurease on these properties, a series ofin vivoandin vitroexperiments was performed. In thein vivostudies rats were intragastrically administered NH4Cl alone and in combination with the mucolytic agent, Muco‐Mist, in various dosing strategies and concentrations. It was determined that the intragastric administration of four consecutive doses of a NH4Cl/Muco‐Mist mixture (20 mmol/L/5%) was capable of converting the stomach from a hydrophobic to hydrophilic state as determined by contact angle analysis. Further, the treated rats became more susceptible to the injurious effect of luminal acid as determined by measuring the haemoglobin concentration of a collected gastric perfusate. In thein vitrostudies it was determined that exposure of the hydrophobic surface of a synthetic mucus gel layer to increasing concentrations of NH4Cl (0–20 mmol/L) resulted in a rapid transition to a hydrophilic state and an associated increase in the flux of H+across its surface.Helicobacter pylorimay induce an attenuation in both mucosal hydrophobicity and barrier properties by producing high concentrations of NH+4in the mucus gel layer. The molecular mechanism of this action may be related to the chemical similarities of NH+4and choline‐based phospholipids which contribute to the stomach's hydophobic

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01295.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non‐cirrhotics, the frequency of non‐response to histamine H2‐receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non‐cirrhotic subject.Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre‐transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2‐receptor antagonists in prophylaxis is as y

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01296.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe protective action of mild irritants has been established. However, the mechanisms as to how they antagonize the injurious action produced by the subsequent challenge with an ulcerogenic stimulus are still unclear. The present study examined the different protective mechanisms of an oral administration of the three mild irritants, 20% ethanol, 0.3 mol/L HCl or 5% NaCl against the gastric injurious actions of absolute ethanol in rats. In an attempt to clarify the pathways and mediators involved in the adaptive cytoprotection, [d‐Pro2, d‐Trp7,9]‐substance P (substance P antagonist),Nw‐nitro‐l‐arginine methyl ester (l‐Name), indomethacin, capsaicin, lidocaine, atropine or hexamethonium was given. The protective action of 20% ethanol but not the other two mild irritants, was antagonized byl‐Name, indomethacin and capsaicin, which are the inhibitors of nitric oxide (NO) and prostaglandins (PG) synthesis, and afferent sensory neuron blocker, respectively. Substance P antagonist, lidocaine or atropine given alone, prevented mucosal damage; however, only substance P antagonist enhanced the anti‐lesion action of 20% ethanol, while atropine and lidocaine increased the protective effect of NaCl and HCl. The three mild irritants increased the residual gastric secretion. Only 20% ethanol and 5% NaCl but not 0.3% HCl significantly increased the basal adherent mucus and also attenuated the mucus depletion by absolute ethanol. It is concluded that the cytoprotective action of either ethanol or NaCl seems to be mediated through the increase of residual gastric secretion and adherent mucus. In the ethanol‐treated group, these actions could act through the afferent sensory fibres, with NO and PG as the possible mediators. The antilesion action of HCl is partly contributed by the increase of residual gastric secretion through its dilution action. However, the protective factors and mediators involved in this action need fur

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01297.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe vagus is involved in mediating gastric cytoprotection and adaptive cytoprotection. However, the central and peripheral mechanisms through which the vagus expresses its action are still poorly known. Medullary thyrotropin‐releasing hormone (TRH) plays an important role in the vagal regulation of gastric function. The stable TRH analogue, RX 77368, micro‐injected into the cisterna magna or the dorsal motor nucleus (DMN) of the vagus at a dose that did not influence gastric acid secretion prevented gastric injury induced by intragastric administration of 60% ethanol in conscious or urethane‐anaesthetized rats. The cytoprotective action of TRH is mediated through vagal cholinergic release of prostaglandin E2(PGE2). Prostaglandin E2action is unrelated to changes in gastric mucosal blood flow (GMBF). In addition, other peripheral mechanisms involve calcitonin gene‐related peptide (CGRP) contained in capsaicin sensitive afferent fibres and nitric oxide, both of which mediate the associated increase in GMBF induced by intracisternal injection of RX 77368. These data indicate that medullary TRH induces vagally mediated gastric protection against ethanol lesions. Its action is expressed through the muscarinic dependent release of PGE2and nitric oxide, and efferent function of capsaicin‐sensitive afferent fibres relea

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01298.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThere is increasing evidence for brain regulation of gastroduodenal function and pathological responses. This laboratory has demonstrated a significant role for dopamine (DA) as a modulator of gastrointestinal function and disease. Using models of both acute (ethanol restraint stress; cysteamine) and chronic (iodoacetamide‐induced gastritis) gastroduodenal mucosal injury, as well as tests of gastric secretory function (conscious basal gastric acid secretion; pylorus ligation;ex vivogastric chamber), we have shown that DA, particularly DA1/D1receptor agonists are powerful gastroprotective agents. This action is demonstrable upon peripheral administration as well as central (particularly intramesolimbic) administration. DA1/D1agonists such as SKF38393 and SKF75670C reduce experimental gastric mucosal injury and secretion while antagonists of these receptors, including SCH23390, worsen experimental gastroduodenal lesions and augment secretion. That there exists a significant central component to DA‐induced gastroprotection is demonstrated by data showing that rats assessed as anxiety prone, develop a greater degree of experimentally induced gastric damage, require greater amounts of DA agonists for 50% gastroprotection and respond to exogenous stress challenge with greater central DA turnover and loss, relative to rats assessed as low in anxiety. Very recently, we showed that dopamine D4receptor blockade by clozapine and activation of dopamine D3receptors by 7‐hydroxy‐N,N‐di‐n‐propyl‐2‐aminotetralin (7‐OHDPAT) are also associated with antisecretory and gastroprotective effects. Taken together, these data suggest that: (i) DA is a significant component of endogenous gastroprotection; (ii) central DA, particularly mesolimbic DA, is an important determinant of peripheral gastroduodenal responses to exogenous chemical and stress challenges; and (iii) the hypothesis that several DA receptor subtypes modulate gastroduodenal function and pathology is inc

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01299.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe use of non‐steroidal anti‐inflammatory drugs (NSAID) for treatment of inflammatory conditions is significantly limited by the untoward effects of these compounds on the gastrointestinal tract. While the pathogenesis of ‘NSAID‐gastropathy’ is not completely understood, there is good evidence that the process is directly linked to suppression of prostaglandin synthesis and possibly to neutrophil adherence to the vascular endothelium. Pretreatment of rats with a nitric oxide (NO) donor (sodium nitroprusside) was found to significantly reduce the extent of gastric injury induced by flurbiprofen. We therefore tested the effects of a novel derivative of flurbiprofen. This compound contains a moiety similar to the NO‐releasing moieties found in many organic nitrates. This compound suppressed gastric prostaglandin synthesis as effectively as flurbiprofen, but caused significantly less haemorrhagic damage. The compound was also found not to induce small intestinal injury. Since the compound was found to exert anti‐inflammatory effects comparable with flurbiprofen, NO‐releasing NSAID may represent a novel class of drugs with markedly reduced gastrointe

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01300.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractAdministration ofEscherichia coliendotoxin abolished the acid secretory response induced by a bolus injection of pentagastrin in the continuously perfused stomach of the anaesthetized rat. Likewise, acid secretion stimulated by the continuous intravenous perfusion of pentagastrin was inhibited by administration of interleukin‐1β (IL‐1β). In both cases pretreatment withNg‐nitro‐l‐arginine methyl ester (l‐Name) but not dexamethasone or indomethacin substantially restored the secretory responses to pentagastrin. The actions ofl‐Name were reversed by the prior administration ofl‐arginine but not by its enantiomer d‐arginine. Even thoughl‐Name increased blood pressure, this does not seem to be the mechanism by which endotoxin‐induced acid inhibition was prevented, since similar systemic pressor responses induced by phenylephrine had no such effect. The secretory response elicited by pentagastrin in the isolated lumen perfused stomach of the rat was not influenced by incubation (100 min) with IL‐1β. These observations suggest that the acute inhibition of acid responses to pentagastrin by endotoxin and IL‐1β involves nitric oxide

ISSN:0815-9319    

DOI:10.1111/j.1440-1746.1994.tb01301.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY