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Certain amines and alkaloids, including such drugs as morphine, and curare alkaloids, can displace histamine in granules and cause its release. Antibiotics like polymyxin are also found to stimulate histamine release. Histamine release occurs when allergens bind to mast-cell-bound IgE antibodies.
Histamine release in the brain triggers secondary release of excitatory neurotransmitters such as glutamate and acetylcholine via stimulation of H 1 receptors in the cerebral cortex. Consequently, unlike the H 1 -antihistamines which are sedating, H 3 -antihistamines have stimulant and cognition-modulating effects.
Pain is due to the release of chemicals such as bradykinin and histamine that stimulate nerve endings. [15] Acute inflammation of the lung (usually in response to pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings. [15]
The C3a, C4a and C5a components are referred to as anaphylatoxins: [4] [5] they cause smooth muscle contraction, vasodilation, histamine release from mast cells, and enhanced vascular permeability. [5] They also mediate chemotaxis, inflammation, and generation of cytotoxic oxygen radicals. [5]
Histamine is a weak base (a compound able to react with a hydrogen ion to form an acid) that can link with acid groups within the granules of the mast cells. [8] The mechanism of the displacement theory. The crux of this theory lies in the assumption that histamine liberators release histamine by displacing it from cells.
Mast cell stabilizers are medications used to prevent or treat certain allergic disorders. They block mast cell degranulation, stabilizing the cell and thereby preventing the release of histamine and related mediators. One suspected pharmacodynamic mechanism is the blocking of IgE-regulated calcium channels. Without intracellular calcium, the ...
An H 3 receptor antagonist is a type of antihistaminic drug used to block the action of histamine at H 3 receptors.. Unlike the H 1 and H 2 receptors which have primarily peripheral actions, but cause sedation if they are blocked in the brain, H 3 receptors are primarily found in the brain and are inhibitory autoreceptors located on histaminergic nerve terminals, which modulate the release of ...
However, about 4-12 hours after antigen exposure, a cough and wheezing may persist in the patient, along with swelling and redness of the skin. This is known as the late-phase hypersensitivity reaction which can last from approximately 1-3 days and is caused by the release of additional mediators from the mast cells and basophils. [5]