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PubMed1991

[Effect of isoproterenol on the liberation of histamine from rat lung mast cells].

Rat lung mast cells were stimulated with drugs with distinct mechanisms of action, namely concanavalin A, compound 48/80 ionophore A23187, in the presence of the beta adrenergic agonist (-)isoproterenol. Cells show a high response when they are stimulated with FNa-calcium. Isoproterenol does not inhibit histamine release induced by any stimuli, but enhances the response to concanavalin A and compound 48/80. Results point to the lack of beta activity on rat lung mast cells.

Animals↗
PubMed1976

[Liberation of histamine by anaesthetics (author's transl)].

Injection of Epontol (7 mg/kg i.v.) to male healthy students caused a brief increase in plasma histamine concentration from 0.7 ng/ml to 3.0 ng/ml. Combined injection (7 mg/kg) and infusion of Epontol (21 mg/kg during 15 min) or combined injection of Epontol (7 mg/kg) and suxamethonium (0.5 mg/kg) caused a more prolonged appearance of histamine in plasma without higher maximum concentrations. During anaesthesia with ketamine (Ketanest), halothane or nitrous oxide the histamine concentrations in plasma remained unaltered.

Anesthesia, General↗
PubMed2002

Role of endogenous histamine in altered lung mechanics in rabbits.

BACKGROUND: Unlike the effects of exogenous histamine, those of endogenous histamine on the lung mechanics have not yet been characterized. The site of endogenous histamine liberation by mivacurium was determined, as were the effects of this histamine on the airway and parenchymal mechanics in control rabbits (group C) and rabbits pretreated with H1 and H2 receptor blockers (group AH). The effectiveness of the receptor blockade was ensured by challenges with exogenous histamine. METHODS: Pulmonary input impedance at low frequencies (ZL) was measured in anesthetized mechanically ventilated open-chest rabbits under control conditions and every minute after administration of an intravenous bolus of mivacurium (2 mg/kg) and exogenous histamine (10 microg/kg). Histamine levels were determined in serum samples taken from the carotid artery and jugular vein before and 1, 3, and 6 min after mivacurium injection. Parameters of airway resistance (Raw) and inertance and parenchymal damping (G) and elastance (H) were extracted from ZL spectra. RESULTS: Mivacurium induced significant increases in plasma histamine levels, with the venous concentrations being significantly higher than those in the artery. The mivacurium-induced increase in Raw (28.7 +/- 2.3%; mean +/- SD) in group C was significantly higher than that in group AH (6.6 +/- 3.4%), whereas the responses in G were not inhibited significantly (23.9 +/- 6.9% vs. 15.5 +/- 3.0%). The significant increases in Raw (70.6 +/- 12.6%) and G (21.0 +/- 4.9%) after exogenous histamine administration were virtually completely abolished by antihistamine pretreatment (3.6 +/- 3.7% and 0.3 +/- 2.6%). CONCLUSIONS: After mivacurium administration, endogenous histamine is liberated at least partly in the systemic circulation, and it induces primarily a heterogeneous airway constriction with minor changes in the parenchymal properties. This response was considerably reduced but not abolished by antihistamine pretreatment, a circumstance suggesting that mivacurium may liberate other constrictor mediators that might also contribute to the airway and parenchymal constriction.

Airway Resistance↗
PubMed1976

The effect of prostaglandin on iridial blood vessel permeability.

Light and electron microscopy is used to examine the effect of exogenous PGE1 on the permeability and reactivity of rat iridial blood vessels. Results show that topical PGE1 causes an increase in the permeability of iridial vessles to carbon particles (200 A diameter). The technique of carbon labelling is used to quantitate increases in permeability caused by varying concentrations of PGE1 (0.001-1.0 mg/ml). Regression analysis shows that there is a linear relationship (P less than 0.02) between carbon labelling and PGE1 concentration over the range of concentrations tested. In other experiments rats were treated with the systemic histamine liberator Compound 48/80, or with topical applications of histamine diphosphate in order to examine the effects of exogenous and endogenous histamine upon iridial blood vessel permeability. These procedures produce only minimal labelling of iridial vessels. It therefore seems likely that PGE1 has a direct effect on iridial vessels and does not act indirectly by bringing about the liberation of endogenous histamine.

Administration, Topical↗
PubMed1984

Alterations in histamine and collagen induced in chick embryos by aminoguanidine and 48/80.

The effects of aminoguanidine (a histamine inhibitor) and 48/80 (a histamine liberator) on the levels of histamine, soluble collagen fraction and total collagen in the chick embryos were studied. Histamine content in bones (tibia and femur) and skin markedly increased in the embryos treated with aminoguanidine. Aminoguanidine treatment was followed by a decrease of total collagen and an increase of soluble collagen fraction both in bones and skin. 48/80 did not change the histamine level in the bones but decreased that in the skin. 48/80 administration resulted in an augmentation of the total collagen content in the skin. Both in the skin and bones soluble collagen fraction was found to be lower in 48/80 treated embryos.

Animals↗
PubMedDate not supplied

Mast cells and middle ear effusion.

The mast cell--an important component of connective tissue--carries in its cytoplasmic granules various biologically active substances, such as heparin, histamine, and a broad spectrum of enzymes. This cell type plays a prominent role in inflammatory and allergic conditions. In the middle ear, the mast cells are mainly localized in the pars flaccida of the tympanic membrane and beneath the tracts of secretory and ciliated cells in the middle ear mucosa. Degranulation of the mast cells by the histamine liberator compound 48/80 causes histamine-rich effusion material to accumulate in the middle ear. Plugging of the eustachian tube and/or tympanic isthmus will bring about a similar accumulation. It would thus seem that mast cells in some way participate in the production of middle ear effusion, probably via their potent mediators.

Animals↗
PubMed1985

Suppression of endotoxin-induced corticosterone secretion in rats by H1-antihistamine.

Corticosterone (CS) secretion is stimulated in rats by an intraperitoneal injection of bacterial lipopolysaccharide (LPS) or by subjecting the animals to immobilization stress. LPS injection caused a significant increase in the lung histamine level and a sharp reduction in the number of intact peritoneal mast cells. Injection of compound 48/80, a histamine liberator, provoked an increase in the histamine levels of the blood and lung and a decrease in the number of intact peritoneal mast cells with a concomitant increase in CS secretion. Administration of histamine, at a dose of 10 mg/kg, induced a marked increase in CS release. LPS-induced CS secretion was attenuated by pretreatment with an H1-antihistamine, promethazine (PMZ), whereas an H2-antihistamine, metiamide, had no effect. In contrast, PMZ was ineffective on CS release provoked by immobilization stress. These results suggest that LPS-induced CS release is mediated, in part, by histamine released in the peripheral tissues, whereas an immobilization stress-induced increase is not mediated by the amine.

Animals↗