Blood Histamine Levels Research Articles

Aquagenic urticaria: evidence of cholinergic and histaminergic basis.

Two patients with urticaria evoked at the site of contact of skin with water have been studied. Protection of the skin from contact with water by prior application of petrolatum ointment prevented wealing, but removal of the stratum corneum enhanced wealing. Organic solvents did not themselves evoke wealing, but they enhanced the reaction to subsequent challenge by water. That the release of acetylcholine is an essential step in the pharmacogenesis of wealing in aquagenic urticaria is indicated by the suppressive effect of locally-applied scopolamine on water-evoked wealing. Aquagenic urticaria is also associated with elevated blood histamine levels and degranulation of mast cells in the water-challenged skin. The relationship of acetylcholine and histamine to each other and to contact of water with the skin remains uncertain.

Histamine-releasing properties of hydroxy-9-methyl-2-ellipticinium acetate.

Previous work on Hydroxy-9-methyl-2-ellipticinium acetate indicated a bronchoconstrictor activity which could be partially offset by antagonists of the H1 histamine receptors, and the absence of any direct effect on smooth muscle. OH-9-CH3-2-E at concentrations of 10 micrograms/ml and 500 micrograms/ml produced a moderate and a variable release of histamine when placed in contract with whole human blood and lung fragments, respectively. In addition, at a dose of 3 mg/kg in the guinea pig, pulmonary airway resistance was raised and the blood histamine level lowered. A significant correlation was found between these two effects. These results demonstrate that OH-9-CH3-2-E possesses a histamine-releasing potency which is partly responsible for its bronchial effects, implying that precautions may have to be taken when it is used as a therapeutic agent in sensitive subjects. However, the moderate intensity of this potency has not so far precluded therapeutic use of the preparation.

Antigen-induced histamine release from mast cells and basophils after hydrocortisone and disodium cromoglycate treatment

The effect of drugs applied in the treatment of allergic diseases such as hydrocortisone and disodium cromoglycate-Intal on the release of histamine during immediate allergic response was investigated. Experiments carried out on guinea-pigs showed that after hydrocortisone administration the blood histamine level fell, whereas the histamine concentration in the lung tissue varied, depending on the time of the drug administration in relation to the antigen challenge. Disodium cromoglycate give before induction of an asthma attack in guinea-pigs lowered the histamine level in the blood and in the lung tissue homogenates. Investigations were also carried out on isolated rat mast cells and human basophils. The stabilizing effect of hydrocortisone was much weaker than that of disodium cromoglycate especially regarding mastocytes. It was found that the extent of histamine release from mastocytes and basophils depends on the concentration of the drugs applied and on the type of antigen used for induction of cell degranulation.

Circulating cyclic nucleotides and amines in human cholera.

In order to study the systemic influences and conditions in cholera infection, estimation of the levels of cyclic AMP, cyclic GMP, histamine and serotonin in the peripheral blood during the illness was carried out. Plasma cyclic AMP levels(26 patients) were significantly higher in the acute stage (65.7 ± 43.8 pmol/ml) than that in the convalescent stage (9.3 ± 8.0 pmol/ml) (P<0.001). Corrected cyclic AMP with hematocrit in the acute stage (46.4 ± 28.1 pmol/ml) were also significantly higher than that in the convalescent stage (P<0.001).

Dose-response studies of the suppression of whole blood histamine and basophil counts by prednisone

If some clinical problems (e.g., radiographic contrast media reactions) arise from mediator release by circulating basophils, prednisone's capacity to prevent such is likely to be at least partly related to its suppressive effects on whole blood histamine and basophil levels. To establish an optimal dosage schedule, 15 healthy male volunteers entered a two-phased study to determine (1) the single dose of prednisone required to produce maximal suppression of histamine and basophil levels and (2) the effects of repeated prednisone doses. Parameters monitored were whole blood histamine, quantitative basophil counts, white blood cell (WBC) and differential counts, and plasma prednisone, prednisolone, and cortisol levels. Fifty milligrams prednisone suppressed whole blood histamine levels as much as a larger dose and also showed a marked effect on circulating basophils and other leukocytes. Three 50-mg prednisone doses given at 6-hr intervals had a greater effect on whole blood histamine and circulating leukocytes than fewer doses. Thus, the commonly used empirical prednisone dosage regimen is supported. One implication of the results of this study is that greater suppression of blood basophils and histamine levels might be obtained by administering the last prednisone dose about 6 hr before procedures in which a very rapid release of mediators from basophils is anticipated.

Blood and Mast Cell Histamine Levels in Magnesium-Deficient Rats

The number and morphology of mast cells (MCs) in the duodenal submucosa and the histamine content of blood and isolated peritoneal mast cells were estimated sequentially in male weanling Sprague-Dawley rats magnesium (Mg)-depleted for up to 48 days. Blood histamine levels increased 4--5-fold by 14 days of Mg depletion and subsequently declined to levels similar to those in pair-fed Mg-adequate controls. In the same period, the submucosal MCs continuously increased in number, beginning to plateau at 6--7 times the control number between days 36--48 of Mg deficiency. Massive MC degranulation was seen in the early stages of Mg-depletion but subsided after 16--20 days. Subsequently, the submucosal MCs appeared small and rounded. They showed reduced staining with toluidine blue indicating a deficiency in the mucopolysaccharide component of the storage granules. Histamine content of purified peritoneal MCs from Mg-deficient rats was reduced by 10 days of Mg depletion and remained at or below one-third the control level throughout the depletion period. The data suggest that the MCs remaining or developed during chronic Mg depletion are deficient in their capacity to store and secrete histamine.

Histamine and Ascorbic Acid in Human Blood

Analysis of 437 human blood samples has shown that when the plasma-reduced ascorbic acid level falls below 1 mg/100 ml, the whole blood histamine level increases exponentially as the ascorbic acid level decreases. When the ascorbic acid level falls below 0.7 mg/100 ml, there is a highly significant increase in the blood histamine level. Oral administration of ascorbic acid (1 g daily for 3 days) to 11 selected volunteers resulted in a reduction of the blood histamine level in every instance.

Distribution of histamine and histaminase (Diamine oxidase) in blood of various species

1. In 12 mammalian species, blood histamine levels varied from less than 20–1900 ng/ml. 2. Levels were highest in pig and rabbit, and in both species a high proportion of the histamine was in platelets. In other species, blood levels were generally in the range 20–120 ng/ml. 3. Plasma histamine levels were less than 1 ng/ml in most species; rat was a significant exception, having plasma levels of 17 ng/ml. 4. Plasma histaminase activity varied greatly, but no correlation between blood histamine levels and enzyme activity was observed.

Circulating antibodies and blood histamine in cattle after treatment against hypodermosis

Studies have been made of the effect of treatment with an organophosphorus insecticide on calves with or without Hypoderma infestation. A close relationship has been demonstrated between variations of circulating antibodies and blood histamine levels. It is suggested that histamine is released following an immunological reaction due to the formation of complexes between antigenic proteins of the dying larvae and circulating antibodies. Other etiologic agents such as intrinsic larval toxicity were also examined. The small variations of histamine levels suggest that histamine plays only a minor part in the mediation of symptoms of anaphylaxis often observed in parasitised cattle after preventive treatment against hypodermosis.

Blood histamine levels after exercise testing.

Histamine has been measured in whole blood and in the plasma of twenty-three subjects following exercise testing of seventeen asthmatics and six normal controls. Whole blood histamine rose in both asthmatics and controls and was associated with a concomitant rise in the basophil count. Plasma histamine in the peripheral venous blood only rose in one patient who developed urticaria after exercise.

Histamine levels in blood and other tissues of male and female C3H mice. II. Mice carrying a 3-methyl-cholanthrene-induced tumor [proceedings

Histamine levels in blood and other tissues of male and female C3H mice. II. Mice carrying a 3-methyl-cholanthrene-induced tumor [proceedings

Der Bluthistaminspiegel bei chronischen myeloproliferativen Erkrankungen – Ein Überblick

Since the discovery of a very high blood histamine level in chronic myelocytic leukemia (CML) 1936, the author could ascertain that this parameter is very useful in the differential diagnosis between CML and various "leukemoid" reactions; in the early diagnosis of CML and in the differential diagnosis between CML and other myeloproliferative disorders. Recent researches proved that no correlation exists between blood histamine level and basophil count in the peripheral blood. Further investigations in this field have to clear up the questions whether it is possible by means of repeated controls of the blood histamine level to predict the development of a polycythemia vera into CML or to establish in a case of osteomyelosclerosis that this disease has been Preceeded by A CML.

Biogenic amine levels in acute Babesia bovis infected cattle

Plasma and whole blood from splenectomized calves infected with B. bovis were assayed by fluorimetric techniques for histamine, 5-hydroxytryptamine (5-HT), noradrenaline and dopamine levels. In addition PCV, thrombocyte and parasite counts were also undertaken. Plasma histamine levels rose till day 4 post-infection (p.i.) and were still elevated on day 7 p.i. Wholw blood histamine levels were significantly higher on days 1, 4 and 6 p.i. Plasma 5-HT levels rose to peak levels on day 3 p.i. and were still significantly elevated on day 7 p.i. Whole blood 5-HT levels were significantly higher on days 1 and 2 p.i. but fell to subnormal levels terminally. Dopamine and noradrenaline levels for both whole blood and plasma were unaltered during the disease process. Thrombocyte levels initially rose, reaching maximum values on day 3 p.i. The level fell continuously below normal from day 4 to 7 p.i. The PCV fell continuously from day 1 p.i. The experimental animals suffered a severe and fatal syndrome, all dying 7 days p.i.

A Correlative study of blood histamine and clinico-pathological presentation in vasomotor rhinitis

100 clinically diagnosed cases of vaso-motor rhinitis were investigated for blood histamine level, peripheral blood eosinophil count and nasal smear examination for eosinophils. The blood histamine was found to be raised in 56 cases and an increased eosinophil count in blood and nasal secretions was observed in 29 and 32 cases respectively.

Guanethidine-induced vasodilatation in the rabbit, mediated by endogenous histamine.

1 The effects of guanethidine (0.5-4 mg/kg i.v.) on arterial pressure, hindlimb blood flow and hindlimb vascular resistance (HVR) were studied in unanesthetized rabbits subjected to "total" autonomic block. 2 Evidence that this response was mediated by histamine release was that (a) 3H-labelled histamine levels in the hindlimb venous blood rose substantially after guanethidine; (b) infusion of exogenous histamine caused an inhibition of the guanethidine-induced vasodilatation; and (c) competitive antagonism of the response was obtained with the H2-antagonist burimamide. 3 There was good correlation between the [3H]-histamine ;elease and the time course of the vasodilator response. Glyceryl trinitrate infusions that lowered HVR substantially, did not cause release of histamine. 4 Reserpine, desipramine and indomethacin pretreatment did not alter the vasodilator response to guanethidine. 5 The guanethidine vasodilator response was not influenced by the H1-antagonist mepyramine or by the other H2-antagonists, metiamide or cimetidine. The vascular receptors stimulated by endogenous histamine may be distinctive from those stimulated by exogenous histamine, or the action of guanethidine may involve greater production of histamine at an intracellular site that is more readily reached by burimamide than by the other H2-antagonists.

Blood and urine histamine levels in normal and pathological states as measured by a radiochemical assay

The utility of the enzymatic radiochemical assay of histamine in diagnosing diseases with known abnormalities in histamine production was investigated. Whole blood histamine levels were abnormal only in patients with basophilia, i.e. chronic myelocytic leukemia or polycythemia vera. Histamine was not detectable (< 1 ng/ml) in normal plasma but was detected in plasma of some patients with either mastocytosis or chronic myelocytic leukemia. These patients also had symptoms which could be attributed to histamine release as, for example, hyperchlorhydria and hypotension. Urinary histamine excretion was also abnormally high in these diseases compared to normal subjects (range < 5–42 μg/24 h, n = 31). Patients with systemic mastocytosis had higher urine values (> 150 μg/24 h) than those with cutaneous mastocytosis (39–88 μg/ 24 h), and the urinary histamine excretion appeared to be an index of the severity of the disease. Studies with l-histidine loading suggest that the kidney is one possible source of urinary histamine.

Adrenaline-stimulated, aspirin-sensitive synthesis of histamine in the rat.

The intravenous injection of 10 microgram/kg of adrenaline raised total rat lung histamine from 5.3 +/- 0.7 microgram to 8.4 +/- 0.7 microgram and rat skin histamine from 624 +/- 51 microgram to 835 +/- 85 withing 5 min. These changes were no longer apparent after 10 min. Stomach histamine was raised by a statistically non-significant extent, intestinal histamine was unaffected. Blood drawn 2 min after the injection of adrenaline failed to show an increased content of histamine. Rats given 1 mg/kg of compound 48/80, had greatly elevated levels of histamine in blood, but exhibited no increase in lung histamine. This result, as well as the extent of the increase of histamine observed in skin, which cannot be accounted for in any other way, point towards stepped-up local synthesis as the origin of the effect of adrenaline. Aspirin (20 mg/kg, intravenously, 10 min prior to adrenaline), prevented increases of skin histamine. Evidence suggesting mast cells as the site of action of adrenaline, is discussed.

Endogenous plasma histamine and "hepatogenic" peptic ulcer in liver cirrhosis (author's transl)

Because of its anatomical relationship to the gastrointestinal tract, the normal liver is able to act as a controlling "filter" against the influx of plasma histamine chiefly by uptake and breakdown. This prevents unwanted effects on the systemic circulation. The ability to eliminate histamine from plasma is decreased in cirrhosis. Plasma histamine levels in peripheral venous blood of ten patients with liver cirrhosis and gastric ulcer, proven radiologically and by endoscopy, indicated a significantly higher concentration (1.3 +/- 0.4 micron/1) than in a control group of 16 patients without such disease (0.7 +/- 0.2 micron/1). In a group of patients with fatty liver (stages I-II) there were normal histamine levels (0.7 +/- 0.3 micron/1).

Blood histamine and plasma histaminase level during human pregnancy

Blood histamine and plasma histaminase level during human pregnancy

Histamine levels in plasma, blood, and urine in severe asthma, and the effect of corticosteroid treatment.

Plasma, whole blood, and urinary histamine levels have been determined in 64 normal subjects, in 10 patients with severe asthma, and in 10 control patients with other illnesses. The mean whole blood levels did not differ between the three groups. The mean plasma level in the asthmatics was significantly greater than that of the normal subjects but not of the control patients. The urinary histamine output was lower in the control patients than in the normal subjects but in the asthmatics did not differ from that of the normals. Corticosteroid therapy caused a marked fall, often to barely detectable levels, of the whole blood histamine concentration of the asthmatic patients and restored the plasma levels to normal but did not affect urinary histamine levels.