Protective Effect of Cimetidine on Aspirin-Induced Gastric Mucosal Damage

Mackercher, Peter A.

doi:10.7326/0003-4819-87-6-676

Cited by 72 publications

(8 citation statements)

References 19 publications

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“…Several studies have made use of transmurat potential difference measurements to detect damage to the gastric mucosal barrier [2,4,13,18,22]. These studies have shown that aspirin, ethanol and bile acids cause a decrease in gastric PD, which coincides with ultrastructural changes of the gastric mucosa [2].…”

Section: Discussionmentioning

confidence: 99%

Esophageal transmural potential difference in patients with symptomatic gastroesophageal reflux

Eckardt

Adami

1980

Klin Wochenschr

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Esophageal electrical potential difference (PD) was studied in 9 patients with symptomatic gastroesophageal reflux and in 9 healthy control subjects. None of the patients revealed gross mucosal damage by radiography or endoscopy, but all of them showed positive acid perfusion studies. In the stomach and across the lower esophageal sphincter PD profiles were remarkably similar in patients and controls. Throughout the lower esophagus however, PD values were slightly higher in patients with symptomatic reflux than in healthy volunteers. These data are in contrast to a previous investigation, in which patients with reflux-induced gross mucosal damage revealed a decreased PD in the lower esophagus. Thus it is concluded that PD measurements of the lower esophagus do not appear to be a valuable test in the differentiation of chest pain of cardiac and esophageal origin.

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Section: Discussionmentioning

confidence: 99%

Esophageal transmural potential difference in patients with symptomatic gastroesophageal reflux

Eckardt

Adami

1980

Klin Wochenschr

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“…Cytoprotection is vaguely dose-related, but so is gastric secretory inhibition, and with the lowest dose of misoprostol significant protection is questionable (26). The H2-receptor antagonists can protect similarly (27).…”

Section: Cy Toprotectionmentioning

confidence: 99%

Prostaglandins and Peptic Ulcer Therapy

Walt¹

1990

Scandinavian Journal of Gastroenterology

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Walt RP. Prostaglandins and peptic ulcer therapy. Scand J Gastroenterol IYW, The expectation that prostaglandin analogues would improve the ulcer healing abilities of other agents by combining mucosal protection with decreased acid secretion has been proved unwarranted. The ulcer healing capabilities of these drugs reflect their antisecretory potency. A role for these drugs in ulcer healing is questionable but their use has been advocated most strongly to prevent ulceration developing during treatment with non-steroidal anti-inflammatory drugs. While some evidence supports this role, an important clinical benefit of reducing complication rates has yet to be demonstrated. matory drugs; peptic ulcer R. P. Walt, Senior Lecturer in Medicine, Queen Elizabeth Hospital, Birmiizgham BIS 2TH. U . K 25(~uppl 174), 29-36 Scand J Gastroenterol Downloaded from informahealthcare.com by Nyu Medical Center on 07/21/15 For personal use only.

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“…While cimetidine protected gastric mucosa against aspirininduced injury, it did not prevent the fall in PD induced by aspirin in man; but because of the initial rise, PD values did not fall below control baseline levels (MacKercher et al, 1976;. A recent report indicated that oral cimetidine given to rats for two days or more, but not less, reduced coldrestraint lesions in the rat.…”

Section: Discussionmentioning

confidence: 96%

Effect of cimetidine on ion fluxes and potential difference across the human stomach

Ivey¹,

Mackercher²

1978

Gut

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SUMMARY The H2-receptor antagonist, cimetidine, reduces acid output regardless of the means of stimulation. It is not known in man whether this is due entirely to a reduction in acid secretion or whether increased back diffusion of hydrogen ions is also occurring. We studied fluxes of H+, Na+, K+, and Cl -ions after acid instillation into the human stomach in six healthy subjects with and without prior administration of 300 mg cimetidine orally. Potential difference across gastric mucosa was measured continuously throughout each study. Cimetidine caused a significant reduction in hydrogen ion secretion (5 05 mEq per 15 minutes controls versus 2-70 cimetidine, P < 0 05), and consequently a significant reduction in net hydrogen flux into the gastric lumen (2'01 mEq per 15 minutes versus 0-02, P < 0 05). There were no significant differences between sodium ion fluxes in control and cimetidine studies, suggesting that the gastric mucosal barrier remained intact. Cimetidine alone caused a highly significant rise in intragastric pH (to 7) and of potential difference (P < 0 001). Addition of intragastric acid (pH < 1 -0) did not reverse the rise in potential difference caused by cimetidine, suggesting that factors other than change in intragastric pH were involved. In conclusion, our studies support the concept that reduction in acid output by cimetidine is due to inhibition of acid secretion, and not to increased permeability to hydrogen ion.Changes in acid secretion cannot satisfactorily explain gastric mucosal damage associated with conditions such as gastric ulcer or acute aspirininduced mucosal damage. The ill-defined concept of mucosal resistance has long been used to explain such cases. An attempt to define and measure this resistance objectively was the 'gastric mucosal barrier' concept popularised by Davenport (1970); Ivey (1971); Code et al. (1963);and Reitemeier et al. (1957). Davenport found that topical aspirin induced an increase in the net fluxes of Na+ ions into the gastric lumen and at the same time of H+ ions out. Increased net movement of Na+ ions into the lumen and of H+ ions out was termed 'alteration' or 'damage' to the 'gastric mucosal barrier' which limited potentially damaging H+ ion movement into the gastric mucosa. In Davenport's studies, alteration of net Na+ and H+ fluxes was associated with a fall in PD. Other workers (Chvasta and Cooke, 1972) confirmed this, and so changes in PD became "Address for reprint requests: Kevin J. Ivey,

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Protective Effect of Cimetidine on Aspirin-Induced Gastric Mucosal Damage

Cited by 72 publications

References 19 publications

Esophageal transmural potential difference in patients with symptomatic gastroesophageal reflux

Esophageal transmural potential difference in patients with symptomatic gastroesophageal reflux

Prostaglandins and Peptic Ulcer Therapy

Effect of cimetidine on ion fluxes and potential difference across the human stomach

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