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Results for “COMPOUND 48-80”

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At least 91 records · Page 5Linked to original sources
PubMed1977

The effect of beta-adrenergic blocking drugs and inhibitors of phosphodiestease on histamine release from isolated mast cells.

Differences in the histamine liberation from isolated rat mast cells after beta-adrenergic blocking drugs were demonstrated. In equimolar concentrations histamine release was induced by Kö 1124, Kö 1500, Kö 1560, Kö 1561 and propranolol. Alprenolol, oxprenolol, propranolol, and trimepranol significantly decreased thehistamine release induced by compound 48-80. The release of granules from cells was inhibited quantitatively more than the release of histamine. This enabled us to surmise the selective effect of beta-adrenergic blocking drugs on cell membranes of mast cells. The possible mechanisms of release reaction are discussed.

Adrenergic beta-Antagonists↗
PubMed1972

Mast cells from human respiratory tissue and their in vitro reactivity.

Human respiratory mast cells, which were obtained coincidentally with diagnostic bronchial brush biopsy, were maintained under conditions for short-term tissue culture. Most mast cells were viable and degranulated on exposure to antibody to immunoglobulin E or to the mast cell degranulating agent compound 48-80. The degranulation of human mast cells is characteristically an intracellular process with no extracellular extrusion of granules.

Animals↗
PubMed1989

Adrenal mast cells modulate vascular and secretory responses in the intact adrenal gland of the rat.

Mast cells were identified in the rat adrenal gland, located in the walls of arterioles at the point at which they penetrate the connective tissue capsule. The mast cell products, histamine and serotonin, both caused dose-dependent increases in rates of perfusion medium flow and steroid secretion in the isolated, perfused rat adrenal gland in situ. Compound 48-80, a mast cell degranulator, caused a significant increase in perfusion medium flow rate and steroid secretion by the in-situ perfused rat adrenal. Administration of disodium cromoglycate, a mast cell stabilizer, before administration of ACTH(1-24) virtually abolished the normal flow rate increment and significantly attenuated the corticosterone secretory response to ACTH(1-24). These observations strongly suggest that adrenal mast cells modulate both vascular and secretory responses in the intact adrenal gland of the rat.

Adrenal Glands↗
PubMed1990

[Histamine and early ischemic arrhythmia in anesthetized cats].

Ligation of left anterior descending coronary artery caused various arrhythmias and reduced histamine content in ischemic myocardium in anesthetized cats. Intracoronary injection of compound 48-80 100 micrograms shortened the onset of VT and VF from 13 +/- 5, 18 +/- 5 min (n = 7) in control to 7.2 +/- 1.1 (P less than 0.01), 11 +/- 5 min (P less than 0.05) (n = 6) respectively, elevated the histamine concentration of plasma after acute coronary artery occlusion (15 +/- 3, 26 +/- 10 ng/ml, P less than 0.05, before and after ligation respectively). Iv chlorpheniramine (5, 10 mg/kg) or cimetidine (20, 40 mg/kg) dose-dependently reduced arrhythmia score, incidence of VF and mortality after myocardial ischemia, but with little influence on histamine content in ischemic myocardium and plasma. These results suggest that release of histamine from the ischemic myocardium is involved in the generation of early arrhythmias through H1 and H2 receptors in anesthetized cats subjected to acute coronary artery occlusion.

Animals↗
PubMed1986

Conjunctival immediate hypersensitivity: re-evaluation of histamine involvement in the vasopermeability response.

The recent development of a technique for quantitative measurement of conjunctival microvascular permeability has permitted detailed pharmacological evaluation of H1- and H2-receptor involvement in histamine-induced increases in conjunctival microvascular permeability and the role of histamine in microvascular permeability changes associated with immediate hypersensitivity responses in the conjunctiva. The conjunctival microvascular permeability response to histamine appears to be entirely mediated by H1-receptors. Pyrilamine (H1-receptor antagonist) virtually abolished the increase in conjunctival extravascular albumin content produced by graded doses of histamine, whereas cimetidine (H2-receptor antagonist) was ineffective. Moreover, selective histamine H2-receptor agonists did not elicit a dose-dependent vasopermeability response in the conjunctiva. Although H1-receptor blockade essentially abolished the microvascular permeability response to histamine, it only partially attenuated the conjunctival microvascular permeability response associated with immediate hypersensitivity and compound 48-80. It appears that conjunctival inflammation caused by mast cell degranulation comprises both a histaminergic and a nonhistaminergic component.

Albumins↗
PubMed1977

Influence of some inflammatory or antiinflammatory substances on skin biopsies investigated with microcalorimetry and respiratory techniques.

Thermal effects were achieved from skin biopsies (epidermis, corium, subcutis) measured by batch-microcalorimetry, after exposure to potent inflammatory or antiinflammatory substances (compound 48/80, histamine, serotonine and hydrocortisone phosphate). Exothermic effects were achieved from 48-80, histamine and hydrocortisone phosphate, when exposed to the skin and lasting for varying time. From serotonine initial endothermic signals were achieved but after about 50 min there was stabilizing of the thermal reaction at the baseline. To analyze the nature of these non-specific thermal effects, determinations of O2 consumption and CO2 production were performed, using Warburg technique on exactly matched tissue pieces exposed to the same substances and run parallely with the microcalorimetrical determinations. An increased respiration, probably as an indicator of increased metabolism was registrated for all test substances acting on the skin. It felt, that the thermal effects reflect an increased metabolism of the tissue exposed to the test substances.

Basal Metabolism↗