On the histamine-binding property of human serum

Gecse, A; Lonovics, J.; Szekeres, L; Zsilinszky, E.; West, G. B.

doi:10.1111/j.2042-7158.1972.tb08869.x

Cited by 8 publications

(1 citation statement)

References 2 publications

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“…Knowledge about histamine binding to plasma proteins in normal subjects is limited. A peptide responsible for binding histamine dissociates from albumin during coagulation or enzymic digestion [5]. Although the basic quarternary amine structure of neuromuscular blocking drugs should promote their binding to alpha^acid glycoprotein (AAG), both alcuronium and gallamine are bound predominantly by plasma albumin [6].…”

Section: Commentmentioning

confidence: 99%

In Vitro Displacement of Vasoactive Mediators From Plasma Proteins: A Possible Mechanism for Pseudo-Allergic Reactions to Neuromuscular Blocking Drugs

Williams

Shale

1992

British Journal of Anaesthesia

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We have studied the release of prostaglandin F2 alpha (PGF2 alpha) and histamine from serum proteins by neuromuscular blocking drugs using equilibrium dialysis, with tracer quantities of radio-labelled mediators as probes. Small concentrations (0.05-0.25 mmol litre-1) of competitive neuromuscular blocking drugs displaced 16-67% of bound histamine. Greater concentrations of suxamethonium (2 mmol litre-1) were required for histamine displacement (19%). There was a significant release of PGF2 alpha by atracurium 1 mmol litre-1 and pancuronium 0.69 mmol litre-1. These findings suggest an alternative mechanism of histamine release by neuromuscular blocking drugs which may be relevant to adverse reactions during use.

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Section: Commentmentioning

confidence: 99%

In Vitro Displacement of Vasoactive Mediators From Plasma Proteins: A Possible Mechanism for Pseudo-Allergic Reactions to Neuromuscular Blocking Drugs

Williams

Shale

1992

British Journal of Anaesthesia

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Urticaria. An updated review

Monroe¹

1977

Archives of Dermatology

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Urticaria can result from many different stimuli, and numerous factors, both immunologic and nonimmunologic, are involved in its pathogenesis. Most commonly considered of immunologic mechanisms is the type I hypersensitivity state mediated by IgE. Another immunologic mechanism involves the activation of the complement cascade, which produces anaphylatoxins that can release histamine. Immunologic, nonimmunologic, genetic, and modulating factors converge on mast cells and basophils to release mediators capable of producing urticarial lesions. In addition to the clinical and laboratory diagnosis and treatment regimens, we review such mediators as histamine, kinins, serotonin, slow-reacting substance of anaphylaxis, prostaglandins, acetylcholine, fibrin degradation products, and anaphylatoxins that increase vascular permeability and can thereby produce wheals. Special consideration is given to histamine and the factors that regulate is secretory release from mast cells and basophils, including the modulating role of intracellular levels of cyclic adenosine monophosphate.

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Urticaria

Monroe¹

1977

Arch Dermatol

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On the histamine-binding property of human serum

Cited by 8 publications

References 2 publications

In Vitro Displacement of Vasoactive Mediators From Plasma Proteins: A Possible Mechanism for Pseudo-Allergic Reactions to Neuromuscular Blocking Drugs

In Vitro Displacement of Vasoactive Mediators From Plasma Proteins: A Possible Mechanism for Pseudo-Allergic Reactions to Neuromuscular Blocking Drugs

Urticaria. An updated review

Urticaria

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