Decrease In Histamine Content Research Articles

Dynamics of mast cell degranulation in human allergic nasal epithelium after provocation with allergen

The histamine content in the nasal epithelial layer of twenty-five patients with nasal allergy was measured before, 10 min after and 1 hr after nasal provocation with allergen. A decrease in histamine content was observed 10 min after provocation compared to the values obtained before provocation (P less than 0.05). There was a tendency for an increase in the histamine content of the nasal epithelium one hour after provocation when compared with the amounts present 10 min after provocation (P less than 0.1). Mast cells in the nasal epithelial layer of a further five patients were studied by electron microscopy 10 min and 1 hr after provocation. The rate of mast cell degranulation appeared to decrease 1 hr after provocation when compared with 10 min. Our study suggests that some mast cells commence their migration to the nasal epithelial layer over a short time period and that they may play a role in the onset of the allergic nasal reaction in patients with allergic nasal symptoms.

Cutaneous mast cell depletion results from topical corticosteroid usage.

The effect of long-term topical application of corticosteroids on human cutaneous mast cells was examined. Two potent corticosteroids, clobetasol-17-propionate and fluocinonide, produced a greater than 85% decrease in histamine content over a 6-wk treatment period, whereas betamethasone valerate, a less potent corticosteroid, produced a 66% decrease. Electron microscopic examination of the biopsies taken from sites after 6 wk of treatment indicate that the reduced levels of histamine were caused by the depletion of mast cells, as evidenced by: the inability to identify any cells representative of mast cells by detailed electron microscopy of the biopsies; and the marked acellularity around the vasculature where mast cells are certain to be detected. Histamine levels did not begin to decline until after 3 wk of corticosteroid treatment, indicating that corticosteroids are not immediately harmful to mast cells. Electron microscopic examination of biopsies taken at the beginning of treatment and 1 wk later showed normal-appearing mast cells, whereas at 3 wk, a small population of mast cells was detected with features usually associated with degenerating or dying cells. These observations suggest that protracted application of corticosteroids to skin is toxic to mast cells. After discontinuation of treatment, the drug-related atrophy associated with chronic application of potent corticosteroids to skin is rapidly reversed, and skin structure returns to near normal by 14 days. Over this time period, however, histamine levels did not increase and mature mast cells could not be observed by electron microscopy. At 14 days post-steroid treatment, the first signs of cells containing sparse amounts of granules having the characteristics of mast cell granules were seen. We interpret this to represent new mast cells beginning to mature in the skin. By 3 mo, histamine levels returned to normal, demonstrating the reversibility of the steroid-induced mast cell depletion. The studies presented here establish the deleterious effects of long-term topical corticosteroid treatment on cutaneous mast cells, and begin to establish a system in which the development of mast cells in tissue can be investigated.

Radiation effects on mast cells: secretory ability, histamine release and recovery, and cell number.

We studied the effects of irradiation with a single fraction of high-energy electrons, in the absorbed dose range used in radiotherapy, on features related to the rat mesenteric mast-cell (MC) population. Such features were energy dispersive X-ray microanalysis for zinc, light and transmission electron microscopic changes, histamine content, and secretory ability of MCs when exposed to the potent secretagogue 48/80. The observation period was 14 days. Also studied were the effects of radiation on the number and histamine content of free peritoneal MCs. Irradiation-induced decrease in histamine content was delayed for at least two days and the rate of subsequent recovery of mesenteric histamine was approximately 70% below normal. This was corroborated by the findings of necrotic and fragmented mesenteric MCs during the entire experimental period. Fibroblasts and macrophages phagocytosed groups of MC granules as well as individual MC granules. A fraction of the extruded MC granules retained an almost normal appearance. This suggests that they were solubilized unduly slow presumably because the irradiation destroyed the mechanisms and enzymes which normally degrade the heparin-protein granule matrix and its heparin. Moreover, the irradiation suppressed the secretory ability of mesenteric MCs and significantly reduced the number of free peritoneal MCs. The findings indicate that the MC is a remarkably radiosensitive connective-tissue cell.

Budesonide and nasal mucosal histamine content and anti-IgE induced histamine release.

The possible mode of action of the recently demonstrated steroid effect on the immediate type allergic reaction has been studied. The influence of a topical steroid, budesonide, on the nasal mucosal histamine content and anti-IgE induced histamine release was studied in an open study. A 1-week treatment with budesonide, used locally in the nose, was administered to 22 hay fever patients who were studied out of the pollen season. There was a decrease of histamine content after steroid treatment and also a blockade of the anti-IgE mediated histamine release, as shown in an in vitro release procedure. This steroid effect may partly explain the effect of steroids on the immediate reaction, as it has been demonstrated in allergen challenge studies.

Absence of increase of histidine decarboxylase activity in mast cell-deficient W/W mouse embryos before parturition.

The histidine decarboxylase (L-histidine carboxylase, EC 4.1.1.22) activity of whole W/W mouse embryos, which are devoid of mast cells, remained very low and did not show the rapid increase before birth (17-20 days of gestation) seen in wild-type +/+ embryos. During the same period, the histamine content also remained very low and no mast cells were detected in the W/W embryos, in the contrast to the large increase in both histamine content and number of mast cells in wild-type embryos. These findings imply that the histamine in embryos is largely derived from mast cells. In +/+ mice, histidine decarboxylase activity decreased rapidly soon after birth without concomitant decrease in histamine content or number of mast cells, suggesting that the enzyme activity in mast cells is regulated by some unknown mechanism.

Restraint‐induced stress ulcer. II. biochemical and ultrastructural studies of gastric mucosa

AbstractThe aim of these studies was to evaluate the light and electron microscopic changes of the gastric mucosa of restrained rats, and to determine if there were correlations between structural changes, histidine decarboxylase activity, histamine content, and gastric secretion.In areas with high‐grade mucosal lesions, signs of functional hyperactivity of the oxyntic and chief cells and cytoplasmic degranulation of the enterochromaffin‐like cells were observed. These changes were not influenced by vagotomy. The hyperactivity of the chief cells was related to a higher proteolytic activity of the gastric juice and to an increased excretion of uropepsinogen (p<0.01). The hyperactivity of the oxyntic cells was not accompanied by an increase in total acidity, which could be explained by hydrogen ion back‐diffusion through a damaged gastric mucosal barrier. The increase in histidine decarboxylase activity (p<0.01) and the decrease of histamine content (p<0.01) in the glandular mucosa of restrained rats, together with the microscopic and ultrastructural observations, suggest that the early microcirculatory changes are due to local alterations in the metabolism of vasoactive amines.

Early effects of corticosteroids on basophils, leukocyte histamine, and tissue histamine

The comparative effect in 11 atopic subjects of a single intravenous injection of methylprednisolone on sequential studies of blood eosinophils, basophils, leukocyte sensitivity to antigen for histamine release, leukocyte histamine content, and skin histamine was examined. No significant changes occurred in any parameter after placebo treatment. In contrast, 4 hr after intravenous treatment with steroid there were significant decreases in mean eosinophil counts (−95%), basophil counts (−72%), and histamine content of 1 × 10 7 leukocyte samples (−62%). Temporal changes in the latter paralleled alterations in circulating basophil levels. No significant changes occurred in the antigen histamine release sensitivity, or the total skin histamine. Studies over a longer period after steroids in 4 subjects showed eosinophil and basophil levels at a nadir at 8 hr, remaining suppressed for 24 hr, and returned to pretreatment levels by 72 hr. Results suggest that corticosteroids induce a prominent decrease in leukocyte histamine due to a depletion of basophils without a decrease in histamine content per basophil, and that skin tissue histamine stores remain unchanged by such treatment.

Alterations in brain endogenous histamine levels in rats after chronic morphine treatment and morphine withdrawal.

Chronic but not acute treatment with morphine resulted in a significant decrease in the histamine concentration in the rat hypothalamus while a slight decrease was noted in the brain stem and cortex. Naloxone precipitated morphine withdrawal caused a significant decrease in histamine concentration in all three brain regions investigated. Withdrawal of morphine resulted in a further significant decrease in histamine level in the hypothalamus, brain stem and cortex. Substitution of morphine by methadone induced changes similar to these seen in rats chronically treated with morphine alone. The present data suggest that in addition to the other biogenic amines histamine may be involved in the pharmacological effects of morphine.

Decrease in histamine content and decarboxylase activities in an isolated area of the cerebral cortex of the cat

Decrease in histamine content and decarboxylase activities in an isolated area of the cerebral cortex of the cat

Histamine content and synthesis in central and pheripheral nerve structures during stress.

Histamine content and histidine decarboxylase activity in cortex and hypothalamus, together with histamine content in peripheral nervous structures were examined in normal and electrically stressed guinea-pigs. A significant increase in histidine decarboxylase activity in hypothalamus and cortex together with concomitant decrease in histamine content in hypothalamus have been found. Electric shock causes also a decrease in histamine content in spinal cord, spinal ganglia, dorsal roots and sensory nerve. The function of histamine in nervous system is discussed.

IUDs and the Biochemical Responses of the Uterus to Estrogen in Ovariectomized Rats

To investigate the effect of the intrauterine device (IUD) on uterine responsiveness to estrogen as a possible explanation for the IUDs antifertility affect IUDs were inserted into 1 uterine horn of 104 rats 1/2 of whom received a subcutanious injection of .2 mcg extradiol-m-beta 35-90 days after IUD insertion. 6 hours after estrogen injection the animals uterine horns were removed and studied for weight water retention histamine and glycogen concentrations and trypan blue permeability. The presence of the IUD caused an increase in all of the parameters in the ovariectomized control rats. Estradiol administration caused increases in the weight water glycogen and trypan blue parameters and a decrease in histamine concentration. The IUD significatly affected (p less than .01) horn weight glycogen concentration and total histamine but water retention histamine concentration and trypan blue permeability were not significatly affected by the IUD. When the treatments were combined they complemented each others increases in weight and glycogen concentration but caused decreases in water retention and trypan blue permeability. The similarity of the actions of the IUD and estrogen on the uterine parameters studied is striking yet estrogen is necessary for implantation and the IUD prevents it. Therefore the IUDS mechanism apparently does not rely on a general alteration of uterine responsiveness to estrogen.

Uterine histamine in rat deciduomata.

The histamine changes accompanying the growth of decidual tissue were differentiated from the histamine changes occurring as a result of the injury used to elicit this growth. Histamine concentration decreased about 50% in decidual tissue when compared with unstimulated uteri, but total histamine content was elevated in deciduomata, being about 100 % higher than in control horns. The procedure utilized to elicit the decidual reaction consisted of cutting the uterus and then scratching it. The cut increased histamine concentration about 100 %, while the endometrial scratch caused only a slight decrease in histamine concentration. It thus appears that the response to the injury and inflammation involved in producing the decidual reaction was an increase in histamine concentration, while the decidual growth response resulted in a decrease in histamine concentration.