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Results for “HISTAMINE LIBERATION”

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At least 19 recordsLinked to original sources
PubMed1994

Pharmacology of histamine liberation. Cationic amphiphilic drugs and mast cells.

The effect of betaadrenoceptor blocking drugs atenolol and propranolol was studied in both nonstimulated and stimulated isolated rat mast cells. Atenolol did not liberate histamine from non-stimulated mast cells, decreased spontaneous secretion, inhibited 48/80 stimulated histamine release, increased 32P incorporation into membrane phospholipids, decreased membrane fluidisation and decreased arachidonic acid liberation from membrane phospholipids of stimulated mast cells. Propranolol dose-dependently liberated histamine from nonstimulated mast cells and inhibited histamine liberation, it nonsignificantly increased membrane phospholipid turnover but significantly increased membrane fluidisation and inhibited stimulated arachidonic acid liberation in stimulated mast cells. The results indicated the interaction of atenolol and propranolol with mast cell membranes, particularly with the phospholipid bilayer, resulting in a possible inhibition of phospholipase A2 activation. Histamine liberation suggested its displacement from granule binding sites after intracellular propranolol accumulation in mast cells.

Animals↗
PubMed1982

Evidence for intracellular histamine liberation in isolated rat mast cells.

The beta-adrenoceptor blocking drug exaprolol liberated histamine from isolated rat mast cells in a dose- and time-dependent way. Histamine was liberated within seconds and was not followed by a parallel granule liberation. The inhibition of histamine liberation was induced with low temperature, low pH, high concentration of Ca2+, TTD, suramin and EDTA. Subcellular distribution of 3H-exaprolol demonstrated a quantitative relationship between histamine depletion against exaprolol uptake in isolated rat mast cell granules. A nonspecific mechanism of action in the effect of exaprolol on mast cells is discussed. It is proposed that the drug acts on mast cells due to the direct and indirect ion exchange mechanism resulted in disproportion between histamine and granule liberation.

Adrenergic beta-Antagonists↗
PubMed1988

Histamine liberation and membrane fluidisation of mast cells exposed to the beta-adrenoceptor blocking drug propranolol.

Propranolol liberates histamine from isolated mast cells and decreases the uptake of extracellular histamine in a dose-dependent way. Histamine liberation due to propranolol is accompanied by calcium displacement from intracellular storage sites. The significant increase in membrane fluidity due to propranolol is temperature dependent. The perturbation of membranes is most probably the explanation of propranolol's interaction with isolated rat mast cells which results in altered histamine transportation.

Animals↗
PubMed1976

[Specific and non-specific histamine liberation].

Histamine-liberation occurs mainly from the mast cells and basophils, the sitr of synthesis of histamine, and other intermediary substances such as serotonin, S.T.S.A. The possible causes for this histamine-liberation are numerous and varied. Histamine-liberation of immunological order only represents a particular case in this chapter as a whole. The study quite specifically deals with histamine-legeration provoked by the direct pharmacodynamic action of drug substances, in particular those which are used in anaesthesiology. These substances are numerous and act according to two essential mechanisms: action by diffusion in the region of the histamine carrying cell (the case of substances of low molecular weight), enzymatic action on the cell membrane (the case of substances with high molecular weight). From the standpoint of clinical consequences, discrimination between specific and non-specific histamine-liberation is therefore risky. In practice, in the face of a symptomatology of histamine shock, it is necessary to bear in mind what is known of the pharmacological action of the substances used, and on the other hand not to neglect the resources of the history, and to employ the laboratory tests capable of providing arguments for or against anaphylaxis.

Basophils↗
PubMed1990

Histamine liberation as a result of nonreceptor interaction.

The highly lipophilic drug exaprolol liberates histamine from isolated mast cells and decreases the uptake of extracellular histamine in a dose-dependent manner. Intracellular histamine depletion was confirmed by electron microscopy and was accompanied by calcium displacement from intracellular storage sites. The significant decrease in membrane fluidity due to exaprolol was temperature-dependent and was most probably a result of its high membrane affinity and intracellular penetration. Membrane perturbation by exaprolol may account for this nonreceptor interaction. This could contribute to the understanding of adverse reactions to beta-adrenoceptor blocking drugs.

Adrenergic beta-Antagonists↗
PubMed1979

[Inhibition of compound 48--80 induced histamine liberation from mast cells by triton X-100].

Triton X-100 at concentrations preceding those which liberated histamine, produced dose-dependent inhibition of compound 48/80-induced histamine release from rat mast cells. Triton X-100 (0.00002 1/1) depleted ATP content in the mast cells and blocked compound 48/80-induced histamine release. The inhibition of compound 48/80-induced histamine release and depletion of the ATP content in the mast cells was reversed by glucose (10 mmole). It is concluded that inhibition by Triton X-100 of histamine release induced by compound 48/80 is dependent on inhibition of energy production.

Adenosine Triphosphate↗
PubMed1975

The effects of histamine liberators and exogenous histamine on wound healing in rat.

The effects of compound 48/80, adenosine-5-triphosphate (ATP) and exogenous histamine (Hi) on the healing of excised surface wound and tensile strength of surgical skin wound in rat were studied. The chemicals were injected directly into the wound area. 48/80, ATP and exogenous Hi were found to stimulate the wound healing as measured by collagen formation, tensile strength examination and a measurement of the surface circular wound. When given separately, the order of activities was: 48/80 is greater than ATP is greater than Hi; when administered together as a mixture, compound 48/80, ATP and exogenous Hi also accelerated the wound healing. The mixture shortened the healing process by about 5 days as compared with 17 days in control.

Adenosine Triphosphate↗