Experimental studies on the pathophysiology of peptic ulcer disease.
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The pathophysiology of clinical peptic ulcer, which is diverse for duodenal, chronic gastric or stress ulcer in humans, has been only partially elucidated by experimental animal studies. A central role of vascular disturbance and acid back diffusion for human stress and animal stress ulcers is evident, whereas a complex and variable set of functional disorders may relate to duodenal ulcer, though the role of acid is paramount. Mucosal resistance factors are of major importance in all types of ulcer and are of particular interest in chronic gastric ulcer. The importance of selecting, for anti-ulcer drug testing, appropriate ulcer models is emphasized, and more extensive use of chronic experimental ulcer healing rate changes, mucus glycoprotein analysis, and cytoprotective changes is recommended. Novel compounds such as pirenzepine, which act on some muscarinic receptors, will help elucidate ulcer pathophysiology as well as provide medical therapy, particularly since all postganglionic vagal transmitter substances in gastric or duodenal mucosae have not yet been identified.Keywords:
Pathophysiology
Stress ulcer
Animal studies
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Bile acids have experimentally been found to damage the gastric mucosa and, thus, may be involved in stress lesion pathogenesis. We therefore measured intragastric bile acid concentrations in 26 critically ill, artificially ventilated patients. The control group consisted of eight healthy volunteers, whose treatment was similar to that of the patients with respect to bed rest, enteral feeding, and administration of H2-blockers. Gastric contents were aspirated via a gastric tube every hour for 24 h. Patients had higher intragastric bile acid concentrations than healthy controls, whether fasting [median 1.3 mmol/L (range 0.7-2.5) versus 0.3 (0.2-0.5) (p less than 0.05)] or fed via a gastric tube [1.3 (0.4-4.0) versus 0.4 (0.2-0.7) (p less than 0.05)]. Physiotherapy, nursing, and drugs (opiates, benzodiazepines, dopamine, pirenzepine, and metoclopramide) had no detectable influence on intragastric bile acid concentrations and pH in patients. We conclude that patients at risk to develop stress lesions have largely increased gastric bile acid concentrations that probably are due to increased duodenogastric reflux. This might be relevant for stress lesion pathogenesis.
Stress ulcer
Metoclopramide
Pathogenesis
Bile reflux
Enteral administration
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AIM The effects and mechinisms of gastric mucosa protective recipe weibaofang on peptic ulcer were studied. METHODS Eighty patients with peptic ulcer diagnosiscd endoscopically were treated by weibaofang)gastric ulcer 12 patients,duodenal ulcer 28 patients)or cimetidine)gastric ulcer 10 patients,duodenal ulcer 30 patients)at randomized and reexamined and compared 8 weeks late,then followed up for 1 year.The protective effects on enthol induced gastric lesion,the effects on gastric acid,gastric mucus secretion and gastric mucosa PGE2 were studied in Wistar rats)twelve rats in each group).RESULTS The healing rat of peptic ulcer in study group was 75.0% which was compared with the rate in control group 70.0%)P0.05),but the clearance rate of helicobacter pylori)55.0% vs.22.0%),the improvement rate of antral gastritis)50.0% vs.15.0%)and ulcer relapse during 1 year)35.7% vs.82.1%)were significantly better than those in control group.This recipe can protect gastric damages from enthol)lesion index 13.8 ±13.0 vs.75.0 ±33.0 P0.05)and its protective mechinism may be related to the increase of gastric mucus secretion.CONCLUSION Weibaofang can increase the gastric mucus secretion and has an effect on peptic ulcer and lower ulcer relapse.
Peptic
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The pathophysiology of clinical peptic ulcer, which is diverse for duodenal, chronic gastric or stress ulcer in humans, has been only partially elucidated by experimental animal studies. A central role of vascular disturbance and acid back diffusion for human stress and animal stress ulcers is evident, whereas a complex and variable set of functional disorders may relate to duodenal ulcer, though the role of acid is paramount. Mucosal resistance factors are of major importance in all types of ulcer and are of particular interest in chronic gastric ulcer. The importance of selecting, for anti-ulcer drug testing, appropriate ulcer models is emphasized, and more extensive use of chronic experimental ulcer healing rate changes, mucus glycoprotein analysis, and cytoprotective changes is recommended. Novel compounds such as pirenzepine, which act on some muscarinic receptors, will help elucidate ulcer pathophysiology as well as provide medical therapy, particularly since all postganglionic vagal transmitter substances in gastric or duodenal mucosae have not yet been identified.
Pathophysiology
Stress ulcer
Animal studies
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A study of 150 patients with ulcer and 38 healthy persons revealed that duodenal ulcer is characterized not only by an increase of the acid- and pepsin-secretory gastric function but also by a reduction of the resilient-viscous properties of the native parietal mucus. Complex determination of acid and pepsin secretion, rheological properties of the gastric mucus is of high diagnostic and prognostic importance.
Pepsin
Peptic
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The pathogenesis of ulcer disease is complex. The present outline focuses on four main aspects: 1) The mechanisms governing acid production and the role of acid in ulcer disease. 2) The mechanisms regulating mucosal resistance to injury. 3) The association of ulcer disease with antral gastritis and Helicobacter pylori infection. 4) Ulcer disease and non-steroidal antiinflammatory drugs (NSAIDs). The complex mechanisms underlying maintenance of mucosal integrity in the normal state and in ulcer disease are discussed. Acid/peptic activity as permissive factors are related to impaired mucosal resistance due to Helicobacter infection or NSAID intake.
Pathogenesis
Pathophysiology
Permissive
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Atrophic gastritis
Pathophysiology
CagA
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The pathophysiology behind chronic gastric and duodenal ulcer is not fully understood, but may be explained as an imbalance between aggressive and defensive factors acting on or in the mucosa. Medical therapy may aim to reduce the aggressive factors acid and pepsin by compounds that neutralize the acid or inhibit the secretion of acid. Peptic activity is reduced by the high acid pH and also by the inhibition. Another group of compounds increases the mucosal defence by stimulating the secretion of mucus, bicarbonate, and growth of the mucosa, or by forming a protective layer on the ulcer crater. Some compounds affect both the aggressive and defensive factors. All modern compounds heal most ulcers in 4 to 6 weeks, but do not alter the natural history of ulcer disease, as indicated by the high rate of ulcer relapses after cessation of treatment.
Pepsin
Bicarbonate
Pathophysiology
Peptic
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The pathophysiology of gastric and duodenal ulcer disease has two sides: the aggressive attack, principally by the highly corrosive gastric acid; and the defending forces of mucus, mucosal resistance, and other protective substances and functions. This report reviews the roles of both the attacking and defending forces in the pathophysiology of ulcer disease. It also discusses how an early notion of ulcer formation (e.g., the Schwarz dictum of "no acid, no ulcer," first published in 1910) became the slogan by which ulcer disease was understood and from which therapy took its cue. Subsequent work has since found that the Schwarz dictum holds for duodenal ulcer, but not for gastric ulcer. Non-acid mechanisms of ulcer formation--i.e., impairment of at least one of the defending or protective forces--are also described, as are treatment approaches to ulcer disease. Although suppression of acid secretion is a mainstay of treatment, agents that safely and effectively strengthen the defense are being used more frequently. There are signs that the safe limits for acid-suppressing therapy have been reached or passed. On the other hand, the search for therapy that strengthens the defensive factors has only begun.
Pathophysiology
Slogan
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The development of acute stress bleeding in intensive-care patients occurs on a multifactorial basis. The basic mechanism lies in the imbalance between aggressive and protective factors. Most intensive care patients show a reduced acid secretion, a reduction of the gastric mucosal blood flow, and a decreased mucus and bicarbonate secretion. Sucralfate enhances most of the defensive mechanisms. These actions are the pathophysiologic basis of the efficacy of sucralfate in the prevention of stress bleeding. Because sucralfate has only a minor influence on the gastric pH and at the same time has proven bactericidal effects, gastric and gut bacterial overgrowth is significantly reduced. These effects explain the observed differences in mortality between sucralfate and alkalinizing drugs like antacids or H2-antagonists. The indications and limits of sucralfate in stress bleeding prophylaxis are pointed out.
Sucralfate
Pathophysiology
Stress ulcer
Gastrointestinal bleeding
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It has been suggested that the mechanisms of NSAIDs-induced peptic ulcer disease are totally different from those induced by Hp. Although a number of studies have examined the effects of Hp eradication on pathophysiology of NSAIDs-induced ulcer diseases, the results have been controversial. At present, therefore, we do not know whether Hp should be eradicated in Hp-positive NSAIDs-induced ulcer patients. Recent studies have shown that both Hp eradication and NSAIDs treatment increases gastric acid secretion, and often causes mucosal lesions in upper GI tract. Based on this back ground, we have decided to review pathophysiology of the Hp-dependent ulcer, and the NSAIDs-induced ulcer. We also discussed the merit and demerit of Hp eradication on gastric mucosal pathophysiology in Hp-positive, NSAIDs-induced ulcer.
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