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Results for “HISTAMINE LIBERATION”

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At least 865 records · Page 48Linked to original sources
PubMed1988

Fluctuating hearing losses in children can be migraine equivalents.

Fluctuation of hearing thresholds in an already severely to profoundly deaf child constitutes a stressing condition and a therapeutic challenge. Thorough medical inquiries revealed strong histories of migraine headaches in the parents of 13 severely deaf children (mean age: 7 years) and two of them also presented symptoms of migraine. This disease is viewed as a form of a relatively benign cerebral vasospasm causing an intense transitory vasodilatation of the small vessels of the brain and a subsequent sterile inflammatory reaction. Liberation of histamine, serotonin and plasma kinins appear to interfere with the metabolism of nerve cells. All children in our study had suffered from anoxia at birth, a condition related to a depopulation of cochlear brainstem nuclei. Migraines may therefore produce obvious hearing symptoms when vasomotor disturbances occur in already damaged nervous structures. Treatment with propranolol hydrochloride (HCl), a potent beta-blocker, resulted in cessation of hearing fluctuations in all patients and in an improvement of thresholds in two of them. We presented our results, as well as preliminary studies on asphyxiated rats shortly after birth, with transitory artificially induced cerebral vasodilatation.

Animals↗
PubMed1982

Hematologic malignancies occurring in patients with urticaria pigmentosa.

Six patients had hematologic malignancies and coincident urticaria pigmentosa, five with the disseminated maculopapular form and one with the plaque form. Two patients had the juvenile-onset variety; the remainder had the adult eruptive variety. None of the patients complained of symptoms that could be attributed to liberation of histamine. In the two patients with juvenile-onset urticaria pigmentosa, the hematologic malignancies developed at the age of 17 years; one had Hodgkin's disease, and the other had acute myelomonocytic leukemia. In three patients with adult eruptive urticaria pigmentosa, the cutaneous lesions developed within 12 months of the diagnoses of lymphocytic lymphoma (two patients) and evolving myelomonocytic leukemia (one patient). In the remaining patient, cutaneous lesions developed many years before chronic lymphocytic leukemia was diagnosed. None of the patients had systemic mastocytosis. Skin biopsy specimens from all six patients showed an increase in dermal and perivascular round cells, and mast cells were seen in specimens from five of the six patients. In patients who received cytotoxic drugs for the hematologic malignancy, there was no change in the urticaria pigmentosa.

Adolescent↗
PubMed1999

Dexamethasone makes the gastric mucosa susceptible to ulceration by inhibiting prostaglandin synthetase and peroxidase--two important gastroprotective enzymes.

The plausible mechanism by which dexamethasone makes the gastric mucosa susceptible to ulceration has been studied. As acid aggravates ulcer, the role of dexamethasone on acid secretion was first investigated. Dexamethasone stimulates both basal and drug (mercaptomethylimidazole)-induced gastric acid secretion by 100 and 50% respectively in male Wister rats 24 h after intramuscular administration at the dose of 1 mg/kg body wt. This stimulated acid secretion is 93% blocked by cimetidine indicating increased liberation of histamine in the process. Pretreatment of dexamethasone before 24 h produces ulcer in 30% of the pylorus- ligated rats and aggravates the ulcer index by 82% in both pylorus and esophagus ligated rats. The incidence of ulceration in the latter cases is also increased by 25%. As mucosal prostaglandin synthetase and peroxidase play an important role in gastroprotection through biosynthesis of prostaglandin and by scavenging endogenous H2O2 respectively, the effect of dexamethasone on the activities of these gastroprotective enzymes were studied. Prostaglandin synthetase and peroxidase activities of the mucosa are significantly inhibited by 87 and 83% respectively by 24-h pretreatment with dexamethasone. The results indicate that dexamethasone makes the mucosa prone to ulceration by inhibiting the activity of prostaglandin synthetase to block the gastroprotective action of prostaglandin and also by inhibiting the peroxidase, thereby elevating the endogenous H2O2 level to generate more reactive hydroxyl radical responsible for the mucosal damage.

Animals↗