Histamine Effects on H+ Permeability by Isolated Gastric Mucosa

Fromm, David; Silen, Mark L.; Robertson, R

doi:10.1016/s0016-5085(76)80314-9

Cited by 12 publications

(2 citation statements)

References 11 publications

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“…In the absence of junctional integrity,the produced H+would be dissipated both by back diffusion and bicarbonate neutralization through the incompetent junctions . In such a situation the acid secretory rate is greatly reduced and the reduction is accompanied by a very low value of PD and the transmucosal resistance.Furthermore, SEDAR and FORTE(1964)have shown electron microscopic evidence for the structural changes in the junctional complexes which occurred after prolonged incubation in Ca2+-deficient media,lending further support for the physiological data.Regarding the junctional permeability(paracellular pathway), FROMM et al(1976)have shown the interesting fact that histamine induces a decrease in of Ca2+on the submucosal side.…”

Section: Discussionmentioning

confidence: 99%

Ca2+ removal effects on bullfrog gastric mucosa in the presence of drugs.

1980

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Section: Discussionmentioning

confidence: 99%

Ca2+ removal effects on bullfrog gastric mucosa in the presence of drugs.

1980

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“…For example, focal pallor of the mucosa precedes the appearance of superficial erosions induced by salicylate even though measurements indicate an increase in total blood flow of the mucosa [34]. Histamine may also have effects on the mucosa independent of alterations in blood flow [35], but controversy exists over the possible beneficial or detrimental effects of histamine [1].…”

Section: Salicylatementioning

confidence: 99%

Drug‐induced gastric mucosal injury

Fromm

1981

World j. surg.

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Although there is much of anecdotal information about drug injury to the gastric mucosa, only a few agents (e.g., salicylates, nonsteroidal‐nonsalicylate antiinflammatory compounds, and alcohol) have been studied in detail. The presence of acid in the gastric lumen is required for an injurious drug to cause clinically significant injury. Injury occurs as a result of the ability of certain drugs to increase the permeability of the mucosa to its own secreted acid lying within the lumen. As the tissue becomes overwhelmed by the diffusing acid, cell death occurs. Drugs that increase the diffusion of acid also interfere with cellular metabolism, an effect that is independent of the ability of the drug to increase diffusion of acid from the lumen into the tissue. However, when metabolic processes of the mucosa are depressed, the ability of the tissue to buffer diffusing acid is impaired. Thus, the quantity of acid diffusing into the tissue is not as important as the buffering capacity of the mucosa. Most instances of drug‐induced injury are not clinically apparent, yet significant hemorrhage occurs in some patients. Even though the initial episode of hemorrhage may be severe, aggressive nonoperative treatment usually is sufficient, provided the mucosa is no longer exposed to the injurious agent. Only a few patients require operation, the extent of which is still controversial.

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Histamine H1- and H2-receptor blockade does not maintain electrochemical gradients across canine gastric mucosa exposed to bile salt

1982

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We tested the hypothesis that histamine mediates the changes in cation permeability and potential difference characteristics of gastric mucosal barrier disruption. Canine Heidenhain pouches were exposed to 20 mM sodium taurocholate both with and without combined histamine H1- and H2-receptor blockade with diphenhydramine 2 mg/kg and metiamide 10 mumol (2.5 mg)/kg/hr. Histamine-receptor blockade did not attenuate the flux, clearance rate, or permeability of hydrogen ion due to bile salt exposure and had no effect on the fluxes of sodium, chloride, and volume. Although the potential difference was higher with combined histamine-receptor blockade, the fall in potential difference due to bile salt was not attenuated. Using a pH-stat system to measure acid loss with the incremental addition of sodium taurocholate to final concentrations of 0, 5, 10, and 20 mM, we failed to observe any difference between control and histamine-receptor blockade in hydrogen flux or permeability. Increases in gastric blood flow due to intraarterial injection of histamine were attenuated with diphenhydramine, 2 mg/kg. Further attenuation of this vasodilation was observed with the addition of a histamine H2 antagonist but not with increasing the dose of the H1 antagonist to 10 mg/kg. Thus we were unable to document that doses sufficient to antagonize histamine H1 and H2 receptors prevent the increase in sodium-hydrogen flux and decrease in potential difference observed with exposure of the canine stomach to bile salt.

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Histamine Effects on H+ Permeability by Isolated Gastric Mucosa

Cited by 12 publications

References 11 publications

Ca2+ removal effects on bullfrog gastric mucosa in the presence of drugs.

Ca2+ removal effects on bullfrog gastric mucosa in the presence of drugs.

Drug‐induced gastric mucosal injury

Histamine H1- and H2-receptor blockade does not maintain electrochemical gradients across canine gastric mucosa exposed to bile salt

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