[Histamine liberation during ultrasonic treatment].
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A study of the release of histamine from basophils and mast cells is clearly important to understand the mechanisms of activation of these cells and the anti-allergic mechanisms of the drugs in use. Important information has been gained through the study of highly purified rodent mast cells as well as human mast cells and basophils of low purity, in many fields: morphology, triggering mechanisms, degranulation and mediator release. Recent findings obtained with purified human mast cells and basophils could better identify the specific potential mediators of these two cells. Many biochemical events have been associated with anaphylactic mediator release: recent evidence suggested that an elevation of intracellular calcium level was an essential event in the processes by which mediators are released.
We determined the generation and liberation of LTB4 in peripheral granulocytes and the histamine release from basophils in patients suffering from cystic fibrosis (CF, median 17.2 years of age, n = 12). We compared the data with an age matched group of healthy donors (n = 12). All patients suffered from an exacerbation of a chronic pulmonary infection caused by P. aeruginosa. Peripheral granulocytes were stimulated at different days before, during and after antiinfectious treatment with Ca-Ionophore, opsonized zymosan and arachidonic acid. The granulocytes from patients with CF as compared to the control group showed an increased omega-Oxidation of the synthesized LTB4 into 20-COOH- and 20-OH-LTB4 after stimulation with Ca-Ionophore and opsonized zymosan (Ca-Ionophore: ratio of LTB4 versus omega-oxidated products (CF): 0.77 +/- 0.007 mean +/- S.E.M., n = 12, control group: 1.07 +/- 0.1, n = 12, p less than 0.01). Stimulation of the cells with Ca-Ionophore combined with arachidonic acid led to a significantly increased formation of lipoxygenase products in the patient group. No significant differences in the basophil counts were determined between both populations. However, the absolute histamine content per basophil was elevated in the CF group (2.4 +/- 0.3 versus 1.6 +/- 0.2 mean +/- S.E.M., n = 12/12, p less than 0.04). Stimulation of basophils with Ca-Ionophore and anti-IgE leads to a significant higher release of histamine per basophil in CF patients (Ca-Ionophore: 2.6 +/- 0.2 versus 1.3 +/- 0.8 pg/basophil, mean +/- S.E.M., p less than 0.05). These data indicate that basophils in CF may have a greater potential to release mediators. During the antiinfectious treatment a normalization of the altered pattern was observed. Within the CF-groups a strong correlation between the release of LTB4, its metabolites, the histamine release per basophil, the total histamine content and clinical (e.g. pO2 FEV1) and laboratory findings (e.g. IgE and IgG levels, CRP) was established. Our data suggest that the inflammatory process in patients with CF is associated with an alteration of the lipoxygenase pathway and histamine releasability of granulocyte subpopulations which correlates with the clinical signs of inflammation.
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Histamine release is a frequent event in the perioperative period. The reasons for its occurrence are complex; they include pseudoallergic and allergic phenomena--and probably a mixture of both. Some drugs and solvents seem to modulate histamine release induced by other drugs. Thus the terms "specific and nonspecific" or "selective and nonselective" histamine release which have their well appreciated place in experimental immunology and pharmacology should be avoided in describing histamine release responses in clinical conditions. The clinical relevance of histamine release in the perioperative period is considerable and can be compared with that of perioperative thrombosis and thromboembolism. Far too many drugs and anaesthetic and surgical procedures give increased plasma histamine levels; premedication with H1- + H2-histamine receptor antagonists is therefore recommended in patients who have a history of hypersensitivity reactions to intravenous agents; a history of atopy, who are to be given the same drug a few days later, undergo surgery with a high risk of histamine release, are more than 70 years old or are poor risk patients with perioperative cardiac, respiratory or liver failure and shock.
The variations in blood pressure, heart rate and plasma histamine levels were monitored for 10 min in 40 patients at risk of releasing histamine after they had been given 2.5 mg X kg-1 propofol in oil emulsion (n = 20) or 7 mg X kg-1 thiopentone (n = 20). The measurements were carried out before anaesthesia, and 1, 2, 3, 5, 7 and 10 min after injecting the drug. All the patients were premedicated with a specific anti-H1 antagonist only (terfenadine). Histamine was measured by radio-immunology (Immunotech). Two patients from the propofol group and three from the thiopentone group showed minor signs, that may have been linked to a release of histamine. Blood pressure fell in both groups by about 20% (p less than 0.001) within the first minute, becoming stable afterwards. The heart rate did not change significantly. Plasma histamine levels did not change in either group, nor in those patients who had presented a local erythema. Propofol did not seem to induce non-specific histamine release when injected over a period of 60 s in patients at risk of doing so.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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The number of patients clinically suffering from rhinitis and/or asthma is very important in any collective of our society. The usage of drugs with a bronchodilator effect as a symptomatic therapy has been widely studied. However, the appearance of new products which complements the effect of bronchodilator and antianaphylactic union has not been sufficiently studied. The motive of this study is to evaluate the inhibition of histamine as the primary and principal mediator, liberated specifically by the Dermatophagoides pteronyssinus and D. farinae before and four hours after drug administration. Conditions for inclusion were the following: To be affected by rhinitis and/or extrinsic asthma induced by house dust mites. Not to have been previously treated with immunotherapy. Be free of previous prophylactic or symptomatic medication. Prick test positive to house dust mites. Serum IgE concentration higher than 100 U.I./ml. Specific histamine release by antigens with a value lower than 10% of the total histamine. The results obtained were based on 21 patients affected with rhinitis and/or asthma induced by dust mites and show that Procaterol produces a moderate reduction on the liberation of histamine as much as 58.6 and 57.4 for dust mites D. pteronyssinus and farinae respectively, four hours after ingestion.
Histamine release was done by the RIA method with soluble allergen and with allergen fixed to a disc, on 26 subjects who were sensitized to hymenoptera venoms. The correlation was statistically significant (r = 0.58) between the two allergens and between RAST and fixed antigen.
The validity of the histamine releasing test for the diagnosis of cow's milk, soy, and egg protein allergy was checked in 31 infants with clinical features of intestinal protein intolerance. The test was positive in 12 of the infants, but in only 5 resp. 1 among them the prick or the Ouchterlony test were pathological. The remaining 19 infants reacted negatively in all 3 tests and subsequently tolerated oral protein loading. The results indicate the superiority of the histamine releasing test in comparison to the conventional prick- and Ouchterlony test.
The authors examined the changes in the histamine level, DAO (diaminoxidase) activity and N--MT (N-methyltransferase) activity in blood (plasma) and tissues of lung and liver (N--MT was examined only in the indicated tissues) in 105 guinea pigs, 45 of whom were healthy and 60 sensibilised and examined during the anaphylactic shock. It was established that during the acute anaphylactic shock there was demonstrative hyperhistanemia and hyperhistaminasemia, which were not observed during experimental anaphylactic shock with subacute course. The activity of lung and liver N--MT in animals with acute and subacute anaphylactic shock did not differ from that of the healthy guinea pigs. The complete inhibition of DAO activity in healthy animals and those with anaphylactic shock did not induce change in the activity of N--MT as well. The latter did not alter after sharp or high level or moderate elevation of the tissue histamine for several days. This histamine was a specific substrate for this enzyme. N--MT is an inductive enzyme, which apparently does not participate in histamine metabolism during acute and subacute anaphylaxis in guinea pigs. For its change, probably, is necessary longer time.