Histamine in blood

One application of solvent extraction in SFA is the determination of anionic surfactants in water, where methylene blue ion pairs are extracted into chloroform. Another is the determination of histamine in blood serum here, interference is removed by extraction into butanol and back-extraction into an aqueous phase prior to the measurement of histamine by the formation of a fluorescent compound with o-phthalaldehyde. 

The first detector to be used for SFA was a photometer, and photometric determinations still form the vast majority of current methods. Other detectors in common use are UV spectrophotometers, used primarily for pharmaceutical compovmds and for bitterness in beer flame photometers, for potassium and sodium determination fluorimeters, used primarily for measuring low levels of determinants in the presence of interferences, such as the determination of histamine in blood, and vitamins in food extracts and ion-selective electrode and pH detectors. In principle, almost any detector with flow-through capability can be used with SFA systems, and determinations based on densitometry, thermometry, and luminescence have been published, among others. 

Barsoum GS, Gaddum JH. The pharmacological estimation of adenosine and histamine in blood. J Physiol Lond 85 1-14, 1935. 

Histamine in the Blood. After its release, histamine diffuses rapidly into the blood stream and surrounding tissues (12). Histamine appears in blood within 2.5 min after its release, peaks at 5 min, and returns to baseline levels by 15 to 30 min. In humans, the diurnal mean of plasma histamine levels is 0.13 ng/g. In urine, elevations of histamine or metaboUtes are more prolonged than plasma elevations. Consequendy, abnormahties are more easily detected by urinary histamine assay. About one-half of the histamine in normal blood is in basophils, one-third in eosinophils, and one-seventh in neutrophils the remainder is distributed among all the other blood components. Increases in blood histamine levels occur in several pathological... 

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... 

The group C counterirritants methyl nicotinate and histamine dihydrochloride produce vasodilation.24 Methyl nicotinate is a nicotinic acid derivative that produces prostaglandin-mediated vasodilation.46 NSAIDs and aspirin block the production of prostaglandins and decrease methyl nicotinate-induced vasodilation. Application over a large area has been reported to cause systemic symptoms and syncope, possibly due to vasodilation and a decrease in blood pressure.47 Patients should be educated to apply only scant amounts to the affected area to avoid this effect. 

Histamine synthesis in the brain is controlled by the availability of L-histidine and the activity of histidine decarboxylase. Although histamine is present in plasma, it does not penetrate the blood-brain barrier, such that histamine concentrations in the brain must be maintained by synthesis. With a value of 0.1 mmol/1 for L-histidine under physiological conditions, HDC is not saturated by histidine concentrations in the brain, an observation that explains the effectiveness of large systemic doses of this amino acid in raising the concentrations of histamine in the brain. The essential amino acid L-histidine is transported into the brain by a saturable, energy-dependent mechanism [5]. Subcellular fractionation studies show HDC to be localized in cytoplasmic fractions of isolated nerve terminals, i.e. synaptosomes. 

The naturally occurring substance histamine causes blood capillaries to dilate and smooth muscle to contract. Most cells release it in response to wounding, allergies, and most inflammatory conditions. Antihistamines block the production of this substance, thereby combating a painful swelling. 

Histamine is released from whole rabbit blood by both cotton extracts and endotoxins, however, the ability of AECD to release histamine is greater than would be expected from endotoxin content alone. Antweiler (63), however, was unable to show in vivo histamine release by endotoxins obtained from cotton extracts in rabbits nor could he show an acute fall in blood pressure of cats after I.V. endotoxin injection, as occurred with subsequent injections of compound 48/80 or other dust extracts. He concludes that endotoxins are not responsible for any histamine releasing activity of cotton dust. 

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. 

Unwanted effects produced by d-tu-bocurarine result from a nonimmune-mediated release of histamine from mast cells, leading to bronchospasm, urticaria, and hypotension. More commonly, a fall in blood pressure can be attributed to ganglionic blockade by d-tu-bocurarine. 

Mast Cells and Basophils. The chief sites of histamine storage are mast cells in the tissues and basophils in blood. These cells synthesize histamine and store it in secretory granules along with a heparin-protein complex. In response to specific antigens, mast cells or basophils are sensitized. Histamine is then secreted from the storage granules. Besides the histamine stores in mast cells and basophils, there is evidence of non-mast cell histamine in some tissues, particularly gastric and intestinal mucosa (60). 

D-tubocurarine can induce a release of histamine which results in a massive drop of blood pressure, an increase of saliva and mucus secretion and laryn-gal and bronchospasms, which can interfere with the intubation. In patients with asthma bronchiale on an allergic basis the use of this drug should be avoided. Due to its ganglion blocking properties D-tubocurarine can induce a histamine-independent drop in blood pressure. 

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... 

A slow intravenous injection of histamine produces marked vasodilation of the arterioles, capillaries, and venules. This causes a fall in blood pressure whose magnitude depends on the concentration of histamine injected, the degree of baroreceptor reflex compensation, and the extent of histamine-induced release of adrenal catecholamines. Vasodilation of cutaneous blood vessels reddens the skin of the face, while a throbbing headache can result from vasodilation of brain arterioles. Vasodilation is mediated through both Hj- and Hj-receptors on vascular smooth muscle. Stimulation of Hj-receptors produces a rapid and short-lived response, whereas stimulation of H2-receptors produces a more sustained response that is slower in onset. Stimulation of Hj-receptors on sympathetic nerve terminals inhibits the release of norepinephrine and its associated vasoconstriction. 

Histamine is an amine found in the cells of all animals (Figure 15.20). The release of histamine in the body is associated with involuntary muscle contraction and dilation of the blood vessels. Allergic reactions release histamine in the body and produce the accompanying side effects associated with hay fever such as coughing, sneezing, and ruimy nose. These effects can be alleviated with the use of antihistamines. 

Most of the important effects of histamine in allergic diseases, including bronchoconstriction and contraction of the gut, are mediated through HI receptors. Other effects, including the cardiovascular responses, involve both HI and H2 receptors. In man the predominant cardiovascular effect is vasodilatation and a lowering of blood pressure. This response is also responsible for the cutaneous flushing commonly observed with histamine release. The... 

In humans, injection or infusion of histamine causes a decrease in systolic and diastolic blood pressure and an increase in heart rate. The blood pressure changes are caused by the direct vasodilator action of histamine on arterioles and precapillary sphincters the increase in heart rate involves both stimulatory actions of histamine on the heart and a reflex tachycardia. Flushing, a sense of warmth, and headache may also occur during histamine administration, consistent with the vasodilation. Vasodilation elicited by small doses of histamine is caused by H -receptor activation and is mediated primarily by release of nitric oxide from the endothelium (see Chapter 19). The decrease in blood pressure is usually accompanied by a reflex tachycardia. Higher doses of histamine activate the H2-mediated cAMP process of vasodilation and direct cardiac stimulation. In humans, the cardiovascular effects of small doses of histamine can usually be antagonized by Hi-receptor antagonists alone. 

Nearly all opioids induce bradycardia (Bowdle, 1998), most likely mediated via central stimulation of the vagus nerve. Cardiovascular depression associated with most opioids is moderate and only the stronger opioids of the fentanyl group induce a more severe effect. Morphine and some of its analogs induce a non-opioid receptor-mediated release of histamine, which can result in a decrease in blood pressure and compensatory... 

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