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Biomedical subjects

M Radermecker

Publications and source records attributed to M Radermecker.

At least 91 records · Page 5Linked to original sources
PubMed1983

[Serum activity of angiotensin converting enzyme during extracorporeal circulation in man].

Serum activity of angiotensin converting enzyme (ACE) were measured during extra-corporeal circulation in five patients undergoing aorto-coronary bypass surgery. We observed a significant decrease of serum ACE levels in the absence of pulmonary circulation, suggesting that in man the lungs were the major source of circulating ACE. An effective extra-pulmonary liberation of ACE could take place during cardiopulmonary bypass. The levels of serum ACE increased with pulmonary recirculation, but preoperative levels were not reached 24 h later.

Aged↗
PubMed1982

Increased complement-mediated leukocytic histamine release in atopics.

Complement-mediated leukocytic histamine release was compared in normal and atopic subjects using isolated leukocytes or heparinized blood. Leukocytes were treated with zymosan-activated autologous serum, whereas blood was directly incubated with zymosan particles. Histamine released from basophils into the leukocyte supernatant or plasma was measured spectrofluorometrically and expressed in percent of total histamine. In atopics, the mean histamine release (47% for leukocytes and 12% for blood) was significantly higher than in normals (30% and 5%, respectively). Individual variations were large in both groups, and a good concordance was noted between the two techniques. By cross-experiments using activated isologous serum from AB donors instead of autologous serum, it was demonstrated that individual variability was not due to differences in intensity of complement activation. Passive sensitization of normal leukocytes with IgE antibodies increased their ability to release histamine in the presence of activated serum. Thus, high complement-mediated leukocytic histamine release is more commonly found in atopics, and appears to be secondary to an intrinsic abnormality of basophils. It is suggested that complement activation and subsequent inflammation could play, especially in house dust-caused asthma, a more important role than previously appreciated. Moreover, an exaggerated mediator releasability as may occur even in nonatopic subjects, could possibly explain some predisposition to interstitial pulmonary diseases caused by inhalants capable of activating complement.

Adult↗
PubMed1982

[Significance of elevated serum ACE in pneumology].

Angiotensin-converting enzyme (ACE) levels were measured in the serum of patients with various pulmonary affections (sarcoidosis, tuberculosis, anthracosilicosis, cancer, etc.), with diabetes or renal insufficiency, and in 247 healthy subjects. Mean ACE levels (41.5 U/ml +/- 16) were significantly higher in sarcoidosis than in normal controls (22 U/ml +/- 6), high values (greater than or equal to 34 U/ml) being observed in 62 p. cent of cases. In these patients, the ACE tended to become normal in parallel with clinical and radiological improvement in the disease, and to increase again during relapses. In 75 p. cent of sarcoidosis patients there was concordance between the increase in alveolar lymphocytes and that of serum ACE. Elevated ACE levels were noted in only 3 p. cent of non-sarcoidosis pneumopathies, and in 24 and 18 p. cent of diabetes and renal insufficiency cases respectively. In the absence of these two latter affections, measuring ACE levels is of obvious value for the diagnosis and follow-up surveillance of sarcoidosis.

Adult↗
PubMed1981

An in vivo demonstration of the antianaphylactic effect of terbutaline.

Allergen-mediated histamine release was measured on small samples of blood in atopic subjects before and following ingestion of two tablets of terbutaline (5 mg) or placebo. No significant variation of histamine release was observed in the placebo group whereas a statistically significant decrease (maximally 45% of basal value) was found in four of the five patients receiving terbutaline. The mean reduction was about 25% of basal allergen-mediated histamine release. The inhibition was observed 1 hr after taking the drug and persisted for at least 5 hr. Twenty-four hours later the amount of histamine released by antigen was again at its basal value. These data indicate that terbutaline, at what are considered therapeutic doses, has an antianaphylactic action which might be of interest in the treatment of atopic disorders.

Adult↗
PubMed1981

Inhibition of allergen-mediated histamine release from human cells by ketotifen and oxatomide. Comparison with other H1 antihistamines.

We have studied the ability of four H1 antihistamines, ketotifen, oxatomide, clemastine and promethazine, and of disodium cromoglycate (DSCG) to inhibit in vitro histamine release mediated by antigen from passively sensitized human lung and from basophilic leukocytes. Anaphylactic histamine release from human leukocytes is inhibited in a comparable fashion by oxatomide, clemastine and promethazine at concentrations just below those inducing histamine release in the absence of antigen. Ketotifen causes a significantly weaker inhibition without inducing histamine release and DSCG is not at all active in this model. On human lung, oxatomide, clemastine and promethazine give a strong and similar inhibition which is linearly related to the dose. Ketotifen markedly differs in this respect, inhibiting according to a bell-shaped dose-response curve and at concentrations closely comparable to that of DSCG. Thus, we confirm that H1 blockers, such as clemastine and promethazine, inhibit anaphylactic histamine release from basophils and human lung but only at high concentrations which may be cytotoxic. Oxatomide behaves very much like these antihistamines. Ketotifen, on the other hand, gives in both models a different pattern of inhibition, closely mimicking that of DSCG. This suggests that the antianaphylactic activity of ketotifen is not related to its H1 blocker properties and that this effect may be relevant to its therapeutic activity.

Allergens↗
PubMed1981

Depression of neutrophil chemotaxis in atopic individuals. An H2 histamine receptor response.

Neutrophil chemotaxis was compared in normal and atopic individuals using a modified Boyden chamber with as chemotactant, autologous serum either unactivated or activated by zymosan or an endotoxin-containing house dust preparation. A high incidence of defective leukotaxis was found in atopics when cells were opposed to activated serum. The cause of this abnormality is not intrinsic to the leukocytes since random migration and chemotaxis towards unactivated serum were comparable in normal and atopic subjects. The defect persisted when atopic leukocytes were opposed to activated normal serum and the chemotactic response of normal neutrophils was not imparied when tested against activated atopic serum. Leukotaxis was significantly depressed by incubating atopic leukocytes with allergen to which they were sensitized, suggesting an inhibitory effect of mediators of anaphylaxis. Histamine inhibited in vitro neutrophil chemotaxis in normal and atopic subjects. This inhibition was dose-related and significantly more pronounced in atopics. Incubation of atopic leukocytes with an H2 antagonist, cimetidine, was capable of enhancing their chemotactic responsiveness towards activated autologous serum to levels observed in normal controls. In the same conditions, an H1 blocker, promethazine, was without effect. These data indicate that the leukotactic dysfunction of atopic individuals results from an abnormal sensitivity of these leukocytes to histamine which, in the chemotactic chamber, may be released from basophils by products of complement activation and, in some experimental conditions, by antigen to which cells are sensitized.

Chemotaxis, Leukocyte↗
PubMed1980

P1 incompatibility in pigeon breeders.

Pigeon breeders of the P2 blood phenotype may develop anti-P1 haemagglutinins as a consequence of natural immunization to pigeon dust. The half-life of labelled P1 erythrocytes was determined in two P2 pigeon breeders otherwise compatible except for the presence of anti-P1 antibodies and in four compatible controls without anti-P1. The half-life of tagged cells was within the normal range in one breeder but significantly reduced in the other, indicating that P1 incompatibility may occur in vivo. Since anti-P1 antibodies are found in about 20% of P2 pigeon breeders, it is suggested that this group may be prone to developing an incompatibility to transfused P1 red cells.

Animals↗
PubMed1980

[Anaphylactic shock in brown Norway rats with reagins and no precipitins in the blood (author's transl)].

Brown Norway rats have been actively sensitized against hen ovalbumine mixed with anti Bordella pertussis vaccine. After ten to twelve days, IgE are detected in the blood, but no precipitins. Anaphylactic shock induced by i.v. injection of 1 mg.100 g-1 body weight of ovalbumine is caracterized by a vascular collapse, the animal dying in about 15 minutes. This collapse is identical with the same general anaphylactic reaction as observed in the Wistar rats, which have large amounts of precipitins in the blood.

Anaphylaxis↗
PubMed1975

Immunization against avian proteins.

A study of sera of pigeon breeders showed a higher ratio of antibodies with an anti-P1 specificity in those who show clinical signs of allergic origin. By absorption of anti-P1 antibodies it was revealed that there exist in the cells, serum and excrement of pigeons, substances with antigenic properties similar to those of human P1 antigen. Pigeon breeders, and particularly those who show clinical signs of allergy, possess also other antibodies which precipitate specific antigens of pigeon serum.

Animals↗
PubMed1975

Anti-P1 activity in pigeon breeders' serum .

Antibodies against the P1 antigen of the P blood group system have been found in 34% of P2 pigeon breeders' sera and in only 6% of the control group. In pigeon breeders, this anti-P1 activity correlates with immunization to pigeon serum and can consistently be removed by absorption with pigeon erythrocytes, serum or droppings. It is concluded that P1 or a related antigen is present in the pigeon blood and drop-pings and that heavy exposure to pigeon dust, as may occur in pigeon breeders, is one of the factors capable of inducing IgM antibodies to P1 antigen. The clinical importance of this finding remains to be defined.

Animals↗