Gastric Mucosal Mast Cells Research Articles

Diphasic disappearance of metachromasia in the rat gastric mucosal mast cells after a single injection of insulin.

Non-fasted rats weighing 260-384 g were injected with diluted insulin, 1 I. U. each, and the changes in the metachromasia of the mast cells in their gastric mucosa were followed from 35 minutes to five hours after the injection. The metachromasia decreased up to 2.5 hours, increased during the subsequent 3-4 hours, and finally began to decrease again five hours after the injection. The importance of the changes observed in the mucosal mast cells for local histamine liberation and during the stimulation of gastric parenchyma is discussed.

The role of gastric mucosal mast cells during Triton WR-1349 lipemia of rats.

AbstractRats were intraperitoneally injected with 1 × 50 mg and 3 × 50 mg of Triton WR‐1339. There occurred steep increase in esterified fatty acids and cholesterol, and the plasma proteins decreased. The mucosal mast cell count and the metachromatic granulation of these cells increased, after a primary decline, in the gastric and jejunal walls under the effect of Triton. The bearing of the phenomenon on hyperlipaemia is considered in the discussion, bringing up the potential inhibition of heparin release.

The Role of Gastric Mucosal Mast Cells during Triton WR-1349 Lipemia of Rats

Rats were intraperitoneally injected with 1 × 50 mg and 3 × 50 mg of Triton WR-1339. There occurred steep increase in esterified fatty acids and cholesterol, and the plasma proteins decreased. The mucosal mast cell count and the metachromatic granulation of these cells increased, after a primary decline, in the gastric and jejunal walls under the effect of Triton. The bearing of the phenomenon on hyperlipaemia is considered in the discussion, bringing up the potential inhibition of heparin release.

Gastric mucosal mast cells in the common laboratory animals and man

Gastric mucosal mast cells in the common laboratory animals and man

Gastric Mucosal Mast Cells in the Common Laboratory Animals and Man

The mast-cell content of the gastric corpus and antrum mucosa of the frog, mouse, rat, hamster, guinea pig, rabbit, cat, dog, and man was studied with an improved method which increases the specificity of the toluidine blue stain for mast cells. Great variability in the density and distribution of gastric mucosal mast cells was noted in the different species. There appears to be no relationship between the known sensitivity of the stomach of a given species to histamine stimulation and its mast-cell content. None of the species demonstrated a topographic association between mucosal mast cells and parietal cells. The notion that endogenous histamine released frommucosalmast cells ultimately causes acid secretion cannot be supported by our data. It is more likely that non-mast-cell histamine is the physiologically active agent.

Protection of the gastric mucosa against the lesions caused by reserpine through degranulation of mucosal mast cells.

AbstractThe ulcerating effects of reserpinisation in the gastric mucosa of rats were studied by special observation of the function of the gastric mucosal mast cells and the changes in mitotic activity of the epithelial cells. The significance of degranulation of the mucosal mast cells for the ulcerating effect of reserpine was also studied after the pretreatment of rats with dexamethasone. Immediately after the dexamethasone treatment there was a pronounced decrease in mitotic count of the gastric mucosal epithelium which 2—3 days later when the mast cells of the gastric mocusa were almost completely degranulated was followed by a 2—3 fold increase in mitotic activity as compared with controls. 10 and 20 days later the mitotic count in the gastric mucosal epithelium decreased below the controls values, the mucosal mast cells being re‐granulated over the control values. The changes in mitotic count in the epithelium of duodenum. ileum and colon under the same conditions were scanty. The degranulation of the mast cells was markedly slighter in the intestinal than in the gastric mucosa. In the reserpinized rats the number of mitoses in the gastric epithelium decreased simultaneously with the degranulation of the mast cells. The degranulation of the mast cells in the duodenal mucosa was slighter and no changes in mitotic activity occurred in the duodenal epithelium. Lesions appeared during reserpinisation in the ventricular mucosa. Reserpinisation after the dexamethasone treatment did not cause ulcer formation in the gastric mucosa, nor did it in this phase cause inhibition in the mitotic activity, typical of which was an overshooting 2—3 days after dexamethasone treatment. The mechanism of gastric mucosal ulceration is discussed.

Different Hormonal Responses of Mast Cells in Gastric Mucosa and Dermis in the Rat

The responses of the gastric mucosal mast cells and the subcutaneous mast cells of the abdominal skin of the rat after administration of ACTH, heparin, and asbestos, were studied. The superficial part of the gastric mucosa contained roughly 5 times as many mast cells as the subcutaneous connective tissue. About three-fourths of the gastric mucosal mast cells were degranulated under the influence of ACTH, but the subcutaneous mast cells showed no changes in number and granulation. The observed difference indicates possibly that mast cells in the gastric mucosa and in the epidermis may have important special, but clearly differing, functions. In the gastric mucosa the sensitiveness of mast cells is possibly connected with their function as a peripheral mediator of stimulation of gastric secretion.

Microcirculatory and mast cell changes in restraint-induced gastric ulcer

Summary Alterations in the microcirculation and mast cell count of the gastric mucosa during the development of gastric ulceration in the restrained rat were studied. The relative blood content of the gastric mucosa was determined by densitometric measurements on thick, cleared sections of hemoglobin-stained gastric tissue. Mast cell enumeration studies were performed on toluidine blue-stained tissue sections. In the unrestrained control rat, blood was fairly uniformly distributed throughout the mucosa. With restraint there was a statistically significant accumulation of blood in the microvessels immediately beneath the surface epithelium, but not deeper in the mucosa. This accumulation occurred during the 'first half hour of restraint and there was no further increase in mucosal blood accumulation with more prolonged restraint. This circulatory change occurred prior to the development of ulceration. When ulceration did occur, the area of erosion involved this hyperemic region of mucosa adjacent to the lumen. Mucosal mast cell counts revealed that with restraint there was a marked decrease in the number of mast cells in the mucosa just below the surface epithelium. This decrease occurred during the first half hour of restraint. The simultaneous mucosal blood accumulation and decrease in mucosal mast cell concentration may be independent. However, vasoactive substances released by mast cell degranulation may be involved in the localized vascular alteration and suggest a new hypothesis concerning the mechanism of stress ulcer: stress → gastric mucosal mast cell degranulation with release of vasoactive substances → gastric mucosal vascular engorgement → decreased resistance to acid-pepsin digestion → mucosal ulceration.

Histidine induced secretion in the pyloric ligated rat stomach.

AbstractThe amount and the pH of the gastric juice in the 1 hr pyloric ligated rat stomach were measured. The amount and the hydrogen ion concentration of the gastric juice were greater when the rats were injected with histidine than with histamine. The pretreatment with 5 times 1 mg of dexamethasone at 12‐hr intervals degranulated the mast cells of the gastric mucosa and increased the pH in the gastric juice. The difference of the secretory activity in histidine or histamine injected rats disappeared after the dexamethasone treatment. The results suggest that the gastric parenchyma is stimulated immediately with histamine formed from histidine and stored in the gastric mucosal mast cell organ.

Effects of dexamethasone, prednisolone and cortisol on the mast cells and tissue eosinophils in rat gastric mucosa.

ABSTRACT Intact rats were injected intramuscularly at 8-hourly intervals with equal amounts, 6×1.0 mg, of dexamethasone (16α-methyl-9α-fluoro-prednisolone) as phosphate, prednisolone (11β,17,21-trihydroxy-pregna-1,4-diene-3,20-dione) and cortisol (11β,17,21-trihydroxy-pregn-4-ene-3,20-dione) both as succinates, all three in water soluble form. The rats were decapitated 4 hours after the last injection and the mucosal mast cells and tissue eosinophilic cells in the body mucosa of the glandular stomach counted. Calculation of the mast cell degranulation and the destruction of tissue eosinophils during the experiment gave the following degranulation coefficients for the degranulation of gastric mucosal mast cells: 0.541 for dexamethasone, 0.177 for prednisolone and 0.088 for cortisol. The corresponding destruction coefficients for the loss of tissue eosinophilia were 0.858, 0.156 and 0.124. It is suggested that the degranulation and destruction coefficients obtained in the investigation are correlated with the catabolic biological activity of the glucocorticoids.