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At least 109 records · Page 6Linked to original sources

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↗

[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↗

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↗

Recovery of schistosomula of Schistosoma mansoni from mouse skin: involvement of mast cells and vasoactive amines.

Normal and S. mansoni-infected mice were exposed to the penetration of 250-350 cercariae through one ear. Two days later, when the ear was removed and chopped, 30 to 50% more schistosomula were recovered from the ears of normal mice than from the ears of infected (immune) mice. Administration of cyproheptadine, a histamine-serotonin antagonist (2 mg/kg), 30 min before challenge infection rendered immune mice indistinguishable from normal mice. Partial depletion of histamine by pretreatment with compound 48-80, a histamine releaser (1 mg/kg) 2 days before challenge infection increased the numbers of schistosomula recovered from the ears of both normal and immune mice. These results are interpreted to mean that vasoactive amines released by skin mast cells play an important role in hindering the viable passage of schistosomula through the skin of normal and immune mice.

Animals↗

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↗