Blood Histamine Levels Research Articles

Desialylated transferrin in plasma of patients with migraine without aura

Patients with migraine, without aura (MO), either during or between attacks, present elevated histamine levels in platelet-poor plasma but normal whole blood histamine levels, compared with controls. This finding is usually interpreted as an increased histamine release from basophils due to unidentified histamine-releasing factors. Compared with 10 control plasma samples, each sample from 12 MO patients (5 during and 7 between in attacks) contained normal amounts of iron and immunologically reactive transferrin but decreased transferrin iron-binding capacity. As transferrin inhibits histamine release in vitro, such as functional abnormality, probably due to modifications of the transferrin glycan moiety (desialylated transferrin), may well account for the increased histamine release observed in MO patients. We suggest that glycan-modified transferrin may be related to migraine histamine-releasing factors.

Twenty-four-Hour Rhythmic Variations of Histamine in Human Female Blood

We have previously observed that blood histamine levels undergo rhythmic 24 hour variations in male normal subjects. In the present study we examined whether similar 24 hour modifications were also present in female subjects. To this purpose, 60 healthy cycling women were enrolled for a chronobiological transverse study. To achieve experimental conditions as homogeneous as possible, the study was carried out on the first day of the menstrual flow. Histamine was determined in whole venous blood by a spectrophotofluorimetric method. The blood histamine levels showed significant rhythmic changes depending on the time of blood sampling, with 1 maximum and 1 minimum within a period of 24 h, with percentage rhythm 15.1, MESOR 0.15 μg/ml, amplitude 0.02 μg/ml and acrophase at 01:20 h. These results reveal the presence of 24 h cyclic variations of histamine levels in the female, as it occurred in male. However, the differences observed in the chronobiological rhythms of histamine between the two sexes may represent a peculiar feature of the first day of the menstrual cycle.

Blood histamine levels in patients with chronic lymphocytic leukemia.

Blood histamine levels in patients with chronic lymphocytic leukemia.

The key role of histamine in the development of atherosclerosis and coronary heart disease

Vitamin C-deficiency is known to cause a disturbance of cholesterol metabolism. Suboptimal plasma ascorbic acid levels also cause increased blood histamine levels, which are exaggerated by sleep-lack and other forms of stress. Histaminemia causes separation of vascular endothelial cells. It is here suggested that the histaminemia of stress and ascorbate depletion combine to cause damage to the arterial endothelium and predispose to atherosclerosis, the principal cause of myocardial infarction.

Cytotoxicity of Vibrio vulnificus cytolysin on rat peritoneal mast cells.

Histamine has been thought to be a permeability enhancing factor in Vibrio vulnificus infection. The injection of living bacteria or purified V. vulnificus cytolysin (VVC) can cause lethality in mice by inducing hemoconcentration and increased vascular permeability. In the present study, we tried to identify whether histamine release causes the increased vascular permeability that is responsible for the lethal effect of VVC. Treatment of rat peritoneal mast cells with high concentrations of VVC caused the release of whole cellular histamine and lactate dehydrogenase (LDH). At concentrations less than 10 HU/ml, histamine and LDH were not released whereas preloaded 2-deoxy-D-glucose was rapidly effluxed with the concomitant decrease in cellular ATP. VVC-treated mast cells were refractory to the stimulation of histamine secretion by Compound 48/80 but remained fully responsive to Ca2+ plus GTP-gamma-S. These results indicate that histamine can be released from mast cells only when the concentration of VVC is high enough to cause the lysis of cells. At low concentrations, VVC does not induce the release of stored histamine from damaged cells. The intravenous injection of 80 HU purified VVC to rats, which can produce the calculated blood concentration of about 3 HU/ml, caused a marked increase in pulmonary vascular permeability, hemoconcentration and death. However, no increase in blood histamine level was detected. This level of VVC in rat blood was enough to cause severe hemoconcentration and lethality but might not be enough to cause cytolysis of the mast cells and resulting histamine release.

Malaises au bain chez le nourrisson, une forme pédiatrique de l'urticaire aquagénique?

Background. — Apparent life-threatening events in infants are a difficult and frequent problem in pediatric practice. The prognosis is uncertain because of risk of sudden infant death syndrome. Case reports. — Eight infants aged 2 to 15 months were admitted during a period of 6 years; they suffered from similar maladies in the bath: on immersion, they became pale, hypotonic, still and unreactive; recovery took a few seconds after withdrawal from the bath and stimulation. Two diagnoses were initially considered: seizure or gastroesophageal reflux but this was doubtful. The hypothesis of an equivalent of aquagenic urticaria was then considered; as for patients with this disease, each infant's family contained members suffering from dermographism, maladies or eruption after exposure to water or sun. All six infants had dermographism. We found an increase in blood histamine levels after a trial both in the two infants tested. The evolution of these “aquagenic maladies” was favourable after a few weeks without baths. After a 2–7 year follow-up, three out of seven infants continue to suffer from troubles associated with sun or water. Conclusion. — “Aquagenic maladies” could be a pediatric form of the aquagenic urticaria.

Bullous delayed pressure urticaria; pressure testing may produce a systemic reaction

We report a patient with bullous delayed pressure urticaria (DPU) and chronic idiopathic urticaria (CIU) in whom a systemic reaction occurred. The reaction occurred 18 h after a pressure test had been performed on the right forearm. Blood histamine levels were more elevated in the sample taken from the forearm on which the test had be applied. Skin biopsy revealed both intraepidermal and subepidermal bullae with a sparse dermal inflammatory infiltrate and direct immunofluorescence showed linear deposition of fibrinogen along the epidermodermal basement membrane. As far as we are aware this is only the third case of bullous DPU reported and the first associated with generalized urticaria and angioedema and severe broncho-obstruction. Possible pathophysiological mechanisms are discussed.

Blood levels of histamine, IL-1 beta, and TNF-alpha in patients with mild to moderate Alzheimer disease.

In this study, we have evaluated the levels of blood histamine, serum interleukin-1 beta (IL-1 beta), and plasma tumor necrosis factor-alpha (TNF-alpha) in 20 patients with mild to moderate Alzheimer disease (AD; 13 early onset and 7 late-onset AD subjects) and in 20 age-matched control subjects (C). AD patients showed higher concentrations of histamine (AD = 452.9 +/- 237.9 pmol/mL; C = 275.3 +/- 151.5 pmol/mL; p < 0.05) and IL-1 beta (AD = 211.2 +/- 31.1 pg/mL; C = 183.4 +/- 24.4 pg/mL; p < 0.01), and lower values of TNF-alpha (AD = 3.59 +/- 2.02 pg/mL; C = 9.47 +/- 2.64 pg/mL; p < 0.001) than elderly controls. Increased levels of histamine and decreased levels of TNF-alpha were observed in both early onset AD (EOAD) and late-onset AD (LOAD) patients, but only EOAD subjects had elevated serum IL-1 beta values compared with age-matched controls. Age negatively correlated with histamine (r = -0.57; p < 0.05) and positively with IL-1 beta levels (r = 0.48; p < 0.05) in healthy subjects, but not in AD, whereas a positive correlation between TNF-alpha scores and age was only found in AD patients (r = 0.46; p < 0.05). Furthermore, histamine and TNF-alpha values correlated negatively in AD (r = -0.50, p < 0.05). In addition, cognitive impairment increased in patients with lower TNF-alpha and higher histamine and IL-1 beta levels, as indicated by the correlations between mental performance scores and histamine (r = -0.37, ns), IL-1 beta (r = -0.33, ns) and TNF-alpha levels (r = 0.42, p < 0.05). Finally, histamine concentrations decreased as depression scores increased in AD (r = -0.63, p < 0.01). These data suggest a dysfunction in cytokine and histamine regulation in AD, probably indicating changes associated with inflammatory processes.

Correlation of blood histamine levels with immunological indices in patients with Schönlein-Henoch purpura.

Correlation of blood histamine levels with immunological indices in patients with Schönlein-Henoch purpura.

Therapeutic effects of CDP-choline in Alzheimer's disease. Cognition, brain mapping, cerebrovascular hemodynamics, and immune factors.

CDP-choline was given to patients with Alzheimer's disease (AD) at a daily dose of 1000 mg/day p.o. for one month. This compound slightly improved mental performance, tended to reduce theta activity in fronto-temporal regions, increasing alpha power in occipital areas, and enhanced cerebrovascular perfusion by increasing blood flow velocity and reducing pulsatility and resistance indexes. In addition, CDP-choline diminished histamine and interleukin-1 levels in blood and serum, respectively, and increased plasma TNF.

Transient increase of blood histamine level induced by pentagastrin. Continuous monitoring by in vivo microdialysis.

Since few studies of (penta)gastrin-induced histamine release from the gastric mucosa into blood has been performed, an effect of pentagastrin on histamine level of rat blood was examined by using the in vivo microdialysis method. Pentagastrin was perfused through the microdialysis probe implanted into the jugular vein of urethane-anesthetized rats or in urethane-anesthetized, totally gastrectomized rats, and dialysis samples of blood were concurrently collected. Histidine decarboxylase (HDC) activities and histamine contents in the glandular stomach and gastric acid output after pentagastrin stimulation were also investigated. Pentagastrin induced a transient increase of blood histamine in a dose-dependent manner but failed to cause any increase of blood histamine in the totally gastrectomized rat. Pentagastrin also induced increases of the HDC activity in the glandular stomach and of the gastric acid output. The peak histamine level in blood occurred 40 min after pentagastrin perfusion, whereas the peak acid secretion occurred after 80-120 min and then leveled off. The transient increase of blood histamine induced by pentagastrin is attributable to the histamine released from enterochromaffin-like cells and could be monitored by using the in vivo microdialysis method.

P-594 - Pentagastrin increases the blood histamine level in the mast cell deficient rat: Continuous monitoring by in vivo microdialysis.

P-594 - Pentagastrin increases the blood histamine level in the mast cell deficient rat: Continuous monitoring by in vivo microdialysis.

Eosinophil cationic protein (ECP), histamine and tryptase in peripheral blood before and during inhalation challenge with toluene diisocyanate (TDI) in sensitized subjects.

To determine whether the measurement of specific markers of inflammatory cells in peripheral blood might be used to detect the inflammatory activity in the airways in asthma induced by toluene diisocyanate (TDI), we measured the levels of eosinophil cationic protein (ECP), histamine and tryptase in peripheral blood before and during inhalation challenge with TDI or methacholine in two groups of subjects who exhibited or did not exhibit an asthmatic reaction after exposure to toluene diisocyanate in the laboratory. When the subjects developed a late asthmatic reaction after exposure to TDI, they showed an increase in their ECP serum levels. By contrast, there were no significant changes in serum ECP levels after exposure to TDI in the control group or after methacholine challenge in either group. Tryptase levels in serum were not detectable before or during inhalation challenge with TDI or methacholine. There was no significant increase in plasma histamine levels during inhalation challenge with TDI or methacholine. These results suggest that eosinophils are 'activated' in subjects who develop a late asthmatic reaction after exposure to TDI and that the measurement of ECP levels in peripheral blood may be a useful marker to monitor airway inflammation.

Open heart surgery increases the levels of histamine in arterial and coronary sinus blood

The possible release of histamine into the coronary circulation during reperfusion of the cold, cardioplegic heart was investigated during open heart surgery in 13 patients (cardioplegic arrest 54 (35-120 min) (median (range)), cardiopulmonary bypass (CPB) 96 (65-360) min. Samples were drawn concomitantly from coronary sinus and arterial blood before cardioplegia and during myocardial reperfusion for measurement of histamine (radioenzymatic method). Additional arterial samples were drawn pre-, per- and postoperatively. CPB induced a sustained increase in arterial histamine (from 4.02 +/- 2.71 nmol/l preoperatively (mean +/- SD) to maximum 16.31 +/- 7.12 nmol/l, p < 0.009). Immediately before cardioplegia histamine levels were higher in arterial than coronary sinus blood (9.24 +/- 4.85 versus 4.04 +/- 2.07 nmol/l, p < 0.002). During myocardial reperfusion coronary sinus histamine increased to levels similar to that of arterial blood. In conclusion, histamine is released during CPB. Before cardioplegic arrest, there is a net uptake of histamine by the heart, which is abolished during reperfusion, possibly due to increased cardiac release of histamine.

Circadian patterns in histamine concentrations and mast cell number in the rat thyroid gland.

We carried out a cross-sectional chronobiological investigation on blood histamine, thyroid histamine and thyroid mast cell number in Wistar rats. Daily, blood histamine varied from 0.38 +/- 0.01 (12.00 h) to 0.60 +/- 0.01 mg/g wet weight (20.00 h) and thyroid histamine from 21.2 +/- 1.19 (04.00 h) to 38.3 +/- 1.54 mg/g wet weight (08.00 h). The number of mast cells per microscopic field ranged from 10.8 +/- 0.6 (16.00 h) to 14.6 +/- 0.6 (12.00 h) in males and from 8.3 +/- 0.2 (04.00 h) to 14 +/- 0.4 (12.00 h) in females. Chronobiologic analysis indicates that the levels of all three variables follow a circadian pattern with a period of 12 h. Peak levels were noted at 07.36 h and 19.36 h for the blood histamine concentration, at 09.00 and 21.00 h for the tissue histamine concentration, and at 11.00 and 23.00 h for the mast cell number. The consistent, consecutive relationship of these data supports the hypothesis that thyroid mast cell number is conditioned by the blood histamine level and thyroid histamine concentration.

Histamine concentration in menstrual and peripheral blood from patients with normal menstrual blood loss and in dysfunctional menstrual bleeding

SummaryMenstrual blood was collected from the uterus within the first 48 hours of the onset of menstrual bleeding from Group 1 (menstrual blood loss 80 ml; n = 20). A peripheral blood sample was collected to coincide with the mid-point in time of the menstrual sample collection. Extracted histamine was condensed to form a fluorophore and its fluorescence was measured by spectrofluorometry. The histamine levels in ng/ml (mean value ± s.d.) for Group 1 were 75.5 ± 34.4 for menstrual blood and 39.6 ± 12.8 for peripheral blood. For Group 2 the histamine levels in menstrual blood were 76.3 ± 33.4 and those for peripheral blood 41.1 ± 14.7. Histamine concentrations for plasma from menstrual blood from both groups were found to be higher than those for peripheral blood (P < 0.0001). No differences were observed between the two groups.

Histamine responsiveness of the various vascular beds of facial and nasal tissues in the dog.

The effects of the close arterial infusion of histamine upon the microcirculation of facial and nasal tissues were examined in dogs. Blood flow through arteriovenous anastomoses (AVA flow), capillaries (CAP flow) and collaterals (COL flow) were determined by electromagnetic flowmetry and the tracer-microsphere technique following an infusion of histamine at doses ranging from 0.5 to 50 nmol/min. Low doses of histamine (0.5-5.0 nmol/min) resulted in an increase in blood flow through the ipsilateral internal maxillary artery (IMA), which could be mainly attributed to a significant elevation of the CAP flow. A concomitant marked increase in AVA flow was observed only after the administration of higher doses (20-50 nmol/min). Significant changes in systemic blood pressure, heart rate and cardiac output occurred only after the infusion of histamine at doses of 20 and 50 nmol/min. Significant increases in the CAP flow of tissues with relatively low perfusion were observed after the infusion of histamine at lower doses. The CAP flow of structures which play an essential role in conditioning the inspired air and exhibit high perfusion rates under control conditions exhibited significant increases only after the administration of higher doses. The present experiments provide direct evidence for a dose-dependent vasodilatory effect of histamine on different microcirculatory compartments of cutaneous and mucosal vascular beds supplied by the IMA in the dog. The results indicate that at low blood histamine levels, an increase in CAP flow predominates, and at higher doses, both elevated CAP flow and elevated AVA flow contribute to the vasodilatory response to histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Daily rhythmic variations in histamine in human blood.

We examined whether or not normal subjects have rhythmic changes of blood histamine levels. Daily predictable variations are present with 3 maxima and 3 minima and acrophase at 09.13. The significance of these changes is presently unknown.

Antihistamine effects and complications of supplemental vitamin C

In the rat, acute stress induces a rapid mobilization of tissue ascorbate, de novo synthesis of ascorbate in liver, and a rise in plasma and urinary ascorbate levels, culminating in elevated total-body ascorbate levels. In human beings, the enhanced metabolism of ascorbic acid after stress results in a rapid fall in ascorbate stores because of the body's inability to synthesize ascorbate in vivo. The physiologic relevance of these changes has not been established, but Chatterjee et al have postulated that ascorbate mobilization during stress may be a natural defense mechanism for the detoxification of excess histamine, an inflammatory substance that is synthesized and released by most tissues in response to chemical, physical, or immunologic stress. Histamine-induced vasodilation and increased vascular permeability promote the fight-or-flight response and healing. Excess histamine, however, has a negative impact on circulatory and immunologic homeostasis. Chronic administration of 2 g of L-ascorbate per day has significantly lowered blood histamine levels by 40% in healthy adults; this reduction in histamine was inversely related to leukocyte chemotaxis, a measure of immune responsiveness. In this study, we examined whether 500 mg ascorbate daily, a level that could be obtained in a carefully planned diet, had an antihistamine effect

Circulatory depression and ventricular arrhythmias induced by compound 48/80 in anaesthetized rats

The effects of graded doses of compound 48/80 on various cardiovascular and respiratory parameters were studied in pentobarbitone-anaesthetized rats. Following intravenous injections, this compound significantly depressed the mean blood pressure (MBP), left ventricular pressure (LVP) and dLVP/dtmax, and caused ventricular tachycardia (VT) or fibrillation (VF) and death. Heart rate (HR) response were variable, and there were no marked changes in airway resistance or blood gases. Pretreatment of the animals with either cimetidine or diphenhydramine significantly prolonged the time of onset of VT/VF but failed to alter the changes in other circulatory variables. A combination of cimetidine and diphenhydramine significantly alleviated the decreases in MBP and LVP and prevented the occurrence of VT/VF. It is suggested that the circulatory depression and the occurrence of ventricular arrhythmias following the administration of compound 48/80 result from activation of H1- and H2-receptors by elevated blood histamine levels due to release of the amine from tissues.