Histamine pathophysiology

Histamine is one of the first inflammatory mediators that was considered to be important in the pathophysiology of a number of allergic diseases. Histamine is released from basophils and mast cells during hypersensitivity reactions to allergens and, -through activation of different receptor subtypes-, may provoke opposite effects on immune and inflammatory responses. While many of the inflammatory effects of histamine are mediated by Hi receptors, H2 receptors may mediate different immunomodulatory responses. This topic was extensively reviewed by Plaut and Lichtenstein (1982) and Falus (1994). 

Brain histamine in pathophysiological conditions and brain diseases... 

The important pathophysiologic mechanism of mast cell and basophil histamine release is immunologic. These cells, if sensitized by IgE antibodies attached to their surface membranes, degranulate when exposed to the appropriate antigen (see Figure 56-5, effector phase). This type of... 

Wherever histamine neurons are involved in pathophysiology, their H3 autoreceptors surely are involved as well. For example, histamine release in the prefrontal cortex is increased during handling stress, and this increase is potentiated when H3 autoreceptors are blocked (Westerink et al. 2002). 

Gothert M, Garbarg M, Hey JA, Schlicker E, Schwartz JC, Levi R (1995) New aspects of the role of histamine in cardiovascular function identification, characterization, and potential pathophysiological importance of H3 receptors. Can J Physiol Pharmacol 73 558-64 Gothert M, Fink K, Frolich D, Likungu J, Molderings G, Schlicker E, Zentner J (1996) Presynaptic 5-HT auto- and heteroreceptors in the human central and peripheral nervous system. Behav Brain Res 73 89-92... 

The histamine system has been implicated in the pathophysiology of schizophrenia by several observations, including evidence for increased CNS metabolism of histamine (Prell et al., 1995), lower levels of H1 receptor expression in the frontal cortex, the striatum, and the thalamus as evaluated by positron emission tomography (Iwabuchi et al., 2005 Yanai and Tashiro, 2007), and the therapeutic efficacy of H3 antagonists on cognitive symptoms in patients with schizophrenia (Vohora, 2004 Esbenshade et al., 2006). Functionally, this... 

Yanai K, Tashiro M. 2007. The physiological and pathophysiological roles of neuronal histamine An insight from human positron emission tomography studies. Pharmacol Ther 113 1-15. 

The pathophysiology of VKC is derived from a combination of type I and IV hypersensitivity reactions.This allergic response involves IgE,Th-2 lymphocytes, eosinophils, mast cells, basophils, neutrophils, macrophages, proin-flammatory cytokines, interleukins, histamine, and other associated mediators. Also involved in this immune response are hormonal and neuroendocrine influences. This immune response results in the clinical manifestations of photophobia, itching, redness, tearing, papillae, corneal vascularization, mucous discharge, and plaque formation. 

Histamine release from mast cells can be caused by a wide variety of basic substances, including mediators such as substance P, bradykinin and venoms such as mastoparan (from wasp venom). It is thought that this interaction involving endogenous mediators is a normal part of pathophysiology involved, for instance, in the triple response in skin. It has been proposed that the non-receptor-... 

The pathophysiology of this disease is early-phase inflammation after allergen exposure (Fig. 3), in which increased binding of IgE on mast cells leads to release of mediators, such as histamine, leukotriene, and cytokines, resulting in acute bronchoconstriction. The cytokines from mast cells are likely to recruit more cells to the airway, such as T lymphocytes, eosinophils, neutrophils, and epithelial cells seen in the late phase of inflammation, leading to airway remodeling and incomplete reversibility. 

Human basophils and mast cells are the only cells expressing the tetrameric high-affinity receptor of IgE (FceRI) and synthesizing histamine [26], Basophils and mast cells (FceRI + cells) play a prime role in the pathophysiology of allergic disorders through the elaboration and release of numerous proinflammatory and immunoregulatory molecules and the expression of a wide spectrum of receptors for cytokines and chemokines [27,28]. 

Some venoms, such as that of the wasp, contain potent histamine-releasing peptides. Since basic polypeptides are released on tissue injury, they constitute pathophysiological stimuli to secretion for mast cells and basophils. Anaphylatoxins (C3a and C5a), which are low-molecular-weight peptides released during activation of complement, may act similarly. 

Histamine is formed from the amino acid histidine and is stored in high concentrations in vesicles in mast cells. Histamine is metabolized by the enzymes monoamine oxidase and diamine oxidase. Excess production of histamine in the body (by. for example, systemic mastocytosis) can be detected by measurement of imidazoleacetic acid (its major metabolite) in tbe urine. Because it is released from mast cells in response to IgE-mediated (immediate) allergic reactions, this autacoid plays an important pathophysiologic role in seasonal rhinitis (hay fever), urticaria, and angioneurotic e ma. Histamine also plays an important physiologic role in the control of acid secretion in the stomach and as a neurotransmitter. 

The so-called histamine headache, which is clinically characterized by a transient, most unilateral, throbbing pain lasting a few hours at the most, is accounted for either by an excessive production of histamine or by hypersensitivity to histamine produced by the body. It is generally combined with facial flush and sensations of heat, sometimes, with epiphora, conjunctivitis, and swelling of the nasal mucous membranes. It can also be induced by intravenous injections of histamine. In some cases histamine desensitization is effective therapy. Pathophysiologically, histamine causes an increase in the cerebrospinal fluid and intraocular pressures. (1768) histamine headache is assumed to be due to the effect of a rise in blood pressure on the carotid arteries which are still atonic following the primary fall in pressure produced by the drug. 

Peters LJ, Kovacic P (2009) Histamine metabolism, physiology, and pathophysiology with applications in veterinary medicine. J Vet Emerg Crit Care 19 311-328. doi 10.1111/j. 1476-4431.2009.00434.x... 

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