Shock histamine

Among the biochemical reactions that ammo acids undergo is decarboxylation to amines Decarboxylation of histidine for example gives histamine a powerful vasodila tor normally present m tissue and formed m excessive amounts under conditions of trau matic shock... 

L-Tyrosine metabohsm and catecholamine biosynthesis occur largely in the brain, central nervous tissue, and endocrine system, which have large pools of L-ascorbic acid (128). Catecholamine, a neurotransmitter, is the precursor in the formation of dopamine, which is converted to noradrenaline and adrenaline. The precise role of ascorbic acid has not been completely understood. Ascorbic acid has important biochemical functions with various hydroxylase enzymes in steroid, dmg, andhpid metabohsm. The cytochrome P-450 oxidase catalyzes the conversion of cholesterol to bUe acids and the detoxification process of aromatic dmgs and other xenobiotics, eg, carcinogens, poUutants, and pesticides, in the body (129). The effects of L-ascorbic acid on histamine metabohsm related to scurvy and anaphylactic shock have been investigated (130). Another ceUular reaction involving ascorbic acid is the conversion of folate to tetrahydrofolate. Ascorbic acid has many biochemical functions which affect the immune system of the body (131). 

Histamine is the biological amine, playing an important role in living systems, but it can also cause unnatural or toxic effects when it is consumed in lai ge amounts. It can occur with some diseases and with the intake of histamine-contaminated food, such as spoiled fish or fish products, and can lead to undesirable effects as headache, nausea, hypo- or hypertension, cai diac palpitations, and anaphylactic shock syndrome. So, there is a need to determine histamine in biological fluids and food. 

Among the biochemical reactions that anino acids undergo is decarboxylation to fflnines. Decar boxylation of histidine, for example, gives histamine, a powerful vasodilator nonnally present in tissue and fonned in excessive fflnounts under conditions of traumatic shock. 

The human histamine Hi-receptor is a 487 amino acid protein that is widely distributed within the body. Histamine potently stimulates smooth muscle contraction via Hi-receptors in blood vessels, airways and in the gastrointestinal tract. In vascular endothelial cells, Hi-receptor activation increases vascular permeability and the synthesis and release of prostacyclin, plateletactivating factor, Von Willebrand factor and nitric oxide thus causing inflammation and the characteristic wheal response observed in the skin. Circulating histamine in the bloodstream (from, e.g. exposure to antigens or allergens) can, via the Hi-receptor, release sufficient nitric oxide from endothelial cells to cause a profound vasodilatation and drop in blood pressure (septic and anaphylactic shock). Activation of... 

Epinephrine (adrenalin) 0.1 to 0.5 mg may be given by subcutaneous or intramuscular injection. Hypotension and shock may be treated with fluids and vasopressors. Bronchodilators are given to relax the smooth muscles of the bronchial tubes. Antihistamines may be given to block the effects of histamine. 

Schaefer U, Schneider A, Rixen D, Neugebauer E (1998) Neutrophil adhesion to histamine stimulated cultured endothelial cells is primarily mediated via activation of phospholipase C and nitric oxide synthase isozymes. Inflamm Res 47(6) 256-264 Schaefer U, Schmitz V, Schneider A, Neugebauer E (1999) Histamine induced homologous and heterologous regulation of histamine receptor subtype mRNA expression in cultured endothelial ceUs. Shock 12(4) 309-315... 

HRA Histamine-releasing activity HRAN Neutrophil-derived histamine-releasing activity HRf Homologous-restriction factor HRF Histamine-releasing factor HRP Horseradish peroxidase HSA Human serum albumin HSP Heat-shock protein HS-PG Heparan sulphate protet ycan... 

Bruising, local irritation, mild pain, erythema, histamine-like reactions, and hematoma can occur at the site of injection. Hypersensitivity reactions involving chills, fever, urticaria, and rarely bronchospasm, nausea, vomiting, and shock have been reported in patients with HIT. Long-term UFH has been reported to cause alopecia, priapism, hyperkalemia, and osteoporosis. 

Schaefer U, Schmitz V. Schneider A. Neugebauer E Histamine induced homologous and heterologous regulation of histamine receptor subtype mRNA expression in cultured endothelial cells. Shock 1999 12 309-315. 

Arnold and Brown (1978) reported on the possibility that bacterial endotoxins, which are widespread, could result in hypersensitivity to histamine. These compounds are complex, heat-stable, lipopolysaccharide materials produced primarily by Gram-negative bacteria. They also reported that endotoxin is known to be capable of inducing histamine release in animals (sometimes called endotoxin shock) similar to that seen in anaphylaxis. Baranowski et al. (1990), however, reported extremely low levels of endotoxin in both good tuna and tuna known to have caused illness in humans. 

Adrenaline (epinephrine) is a sympathomimetic agent that causes bronchodilatation. It is used to relieve bronchospasm in anaphylactic shock reactions. Histamine, kinins and prostaglandins, such as prostaglandin E2, are inflammatory mediators. In response to allergic stimuli, inflammatory mediators may cause bronchoconstrictions. Guaifenesin is an expectorant preparation that increases bronchial secretions to promote the expulsion of the mucus coughed up. 

An important example of PLP-dependent amino acid decarboxylation is the conversion of histidine into histamine. Histamine is often involved in human allergic responses, e.g. to insect bites or pollens. Stress stimulates the action of the enzyme histidine decarboxylase and histamine is released from mast cells. Topical antihistamine creams are valuable for pain relief, and oral antihistamines are widely prescribed for nasal allergies such as hay fever. Major effects of histamine include dilation of blood vessels, inflammation and swelling of tissues, and narrowing of airways. In serious cases, life-threatening anaphylactic shock may occur, caused by a dramatic fall in blood pressure. 

Drug-specific antibodies of the IgE type combine via their Fc moiety with receptors on the surface of mast cells. Binding of the drug provides the stimulus for the release of histamine and other mediators. In the most severe form, a life-threatening anaphylactic shock develops, accompanied by hypotension, bronchospasm (asthma attack), laryngeal edema, urticaria, stimulation of gut musculature, and spontaneous bowel movements (p. 326). 

IgE-mediated allergic reactions (p. 72) involve mast cell release of histamine (p. 114) and production of other mediators (such as leukotrienes, p. 196). Resultant responses include relaxation of vascular smooth muscle, as evidenced locally by vasodilation (e.g., conjunctival congestion) or systemically by hypotension (as in anaphylactic shock) enhanced capillary permeability with transudation of fluid into tissues— swelling of conjunctiva and mucous membranes of the upper airways ( hay fever ), cutaneous wheal formation contraction of bronchial smooth muscle-bronchial asthma stimulation of intestinal smooth musde—diarrhea. 

Hydrocortisone exhibits anti-shock, anti-allergy, and anti-inflammatory action. It raises sugar content in the blood, increases potassium secretion, and lowers sodium excretion from the body. It exhibits anti-metaboUc action and reduces histamine synthesis in the body. 

The vasodilatory effect of Hi-receptor stimulation is mainly due to an endothelial release of nitric oxide, which is able to activate the soluble guany-late cyclase in vascular smooth muscle cells. This effect is mainly responsible for the erythema seen after injection (insect sting) of histamine. Furthermore, it is responsible, together with the increased capillary permeability, for the cardiovascular symptoms seen in anaphylactic or allergic shock. 

The clinical uses of catecholamines are based on their actions on bronchial smooth muscle, blood vessels, and the heart. Epinephrine is also useful for the treatment of allergic reactions that are due to liberation of histamine in the body, because it produces certain physiological effects opposite to those produced by histamine. It is the primary treatment for anaphylactic shock and is... 

Sinus problems, hay fever, bronchial asthma, hives, eczema, contact dermatitis, food allergies, and reactions to drugs are all allergic reactions associated with the release of histamine and other autocoids, such as serotonin, leukotrienes, and prostaglandins. Histamine release is frequently associated with various inflammatory states and may be increased in urticarial reactions, mastocytosis, and basophilia. Histamine also acts as a neurotransmitter in the central nervous system (CNS). Upon release from its storage sites, histamine exerts effects ranging from mild irritation and itching to anaphylactic shock and eventual death. 

Bovet and Staub first described agents that block histamine with the discovery that these agents provide protection against anaphylactic shock. Pyrilamine ma-leate was described as a specific and effective histamine antagonist in 1944. Diphenhydramine and tripelenna-mine soon followed (Babe and Serafin, 1996). 

They are mediated by IgE antibodies. On exposure to the drug, antigen and antibody reaction takes place on mast cells and basophils releasing various mediators e.g. histamine, leukotrienes, 5 hydroxytryptamine (5-HT), prostaglandins etc., which are responsible for immediate immune reactions like skin reaction, anaphylactic shock, asthma etc. These reactions occur immediately after challenge and are termed as immediate hypersensitivity. 

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