Histamine induced edema

Histamine-induced edema results from the action of the amine on Hi receptors in the vessels of the microcirculation, especially the postcapillary vessels. The effect is associated with the separation of the endothelial cells, which permits the transudation of fluid and molecules as large as small proteins into the perivascular tissue. This effect is responsible for urticaria (hives), which signals the release of histamine in the skin. Studies of endothelial cells suggest that actin and myosin within these cells contract, resulting in separation of the endothelial cells and increased permeability. 

As regards the action against histamine-induced edema, S. desoleana oil showed a lower inhibitory effect than S. sclarea oil and chlorphen-amine, used as reference drug [77]. This experimental model of edema, related to the presence of the autacoid histamine alone, does not allow an extensive evaluation of how the oils in question act, because of the short half-life of the edematous agent used. 

Antiinflammatory effects of astramembrannin I (astragaloside IV), isolated from A. membranaceus, were demonstrated in rats. This compound inhibited the increase of vascular permeability induced by serotonin or histamine. Oral administration of astramembrannin I caused a dose dependent reduction in carrageenan-induced edema of the hind paw of rats [15]. 

During the investigation of the effect of intraperitoneal administration of silatrane at a dose of 150 mg/kg per day on the development of histamine-induced experimental ulcers in white rats there have been identified 10 compounds of this class which produce a strong antiulcerous action67. The antiulcerous effect of these compounds is manifested in a lower number of ulcerous injuries and a smaller edema of the mucous membrane of the stomach. The silatranes appear to produce both protective and preventive effects on the development and course of histamine-induced ulcerous process in the stomach. 

It is of interest how the presently accepted concept of aspirin and aspirinlike compounds involvement with PGs came about. The last of the aspirin theories to arise proposed that aspirin interfered with leukocyte migration to the site of injury, thus inhibiting the inflammatory process. A prostaglandin phase of inflammation, where PGs arose in the exudate of experimentally induced edema after the appearance of histamine and bradykinin, was already known. These two events appeared to coincide in the inflammatory process. Thus, the time was ripe. In studying the mediators responsible for the anaphylactic response in sensitized guinea pig lungs, Piper and Vane (1969) isolated histamine, SRS-A, and a new substance they called rabbit aorta contracting substance (RCS), a very unstable material (1 to 2 min) whose release, and presumably production, was selectively inhibited by aspirin-... 

S. sclarea oil was also able to reduce histamine-induced hind paw edema [48] the antiedematous effect increased progressively in time after the administration of the edema-inducing agent and was greater than chlorphenamine, used as antihistaminic reference drug. 

These drugs decrease histamine-induced vasodilatation, edema, and secretion. They may also act at the level of the central nervous system (CNS) to inhibit the reticular activating system. 

This consists of (1) a localized red spot extending for a few millimeters around the site of injection that appears within a few seconds and reaches a maximum in about a minute (2) a brighter red flush, or flare, extending about 1 cm or so beyond the original red spot and developing more slowly and (3) a wheal that is discernible in 1-2 minutes and occupies the same area as the original small red spot at the injection site. The initial red spot results from the direct vasodilating effect of histamine (H -receptor-mediated NO production), the flare is due to histamine-induced stimulation of axon reflexes that cause vasodilation indirectly, and the wheal reflects histamine s capacity to increase capillary permeability (edema formation). 

Fernandes et al. [35] reported that these SQTs were able to inhibit the activation and/or release of inflammatory mediators like bradykinin, platelet activating factor, histamine, IL, IL-1 p, TNFa, and PGE2. They also inhibited the up-regulation of the enzymes COX-2 and iNOS (inducible nitric oxide synthase). a-Humulene stood out in the study as it was the only compound that could, in a systematic treatment, reduce the histamine-induced mouse paw edema and largely prevent both TNFa... 

Mast cell degranulation in response to allergens results in release of mediators such as histamine eosinophil, and neutrophil chemotactic factors leukotrienes C4, D4, and E4 prostaglandins and platelet-activating factor (PAF). Histamine is capable of inducing smooth muscle constriction and bronchospasm and may play a role in mucosal edema and mucus secretion. 

Biogenic amines in wine and fermented foods are formed primarily via the microbial decarboxylation of amino acids. Examples, such as histamine, tyramine, and phenylethylamine are toxic, especially in alcoholic beverages. Ethanol can inhibit the monoamino oxidase responsible for amine detoxification (Maynard and Schenker, 1996). Histamine can induce allergenic reactions in humans, such as rashes, edema, headaches, hypotension. Tyramine and phenylethylamine can cause hypertension and other symptoms related to the release of noradrenaline. 

Cryptolepine has been found to possess anti-inflammatoiy effects in the carrageenan-induced paw edema in rats (27) and Iwu (as cited in Iwu et al 1999) has also reported that the compound has shown histamine antagonism (1). 

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