Biomedical subjects

M C Santos

Publications and source records attributed to M C Santos.

7 recordsLinked to original sources

PubMed1992

Vagal function impairment after exercise training.

The present investigation was undertaken to evaluate the vagal function of trained (T) and sedentary (S) rats by use of different approaches in the same animal. After 13 wk of exercise training (treadmill for 1 h 5 times/wk at 26.8 m/min and 15% grade), T rats had a resting heart rate (HR) slightly but significantly lower than S rats (299 +/- 3 vs. 308 +/- 3 beats/min). T rats had marked reduction of the intrinsic HR (329 +/- 4 vs. 369 +/- 5 beats/min) after blockade by methylatropine and propranolol. They also exhibited depressed vagal and sympathetic tonus. Baroreflex bradycardia (phenylephrine injections) was reduced, bradycardic responses produced by electrical stimulation of the vagus were depressed, and responses to methacholine injection were decreased in T rats. Therefore several evidences of vagal function impairment were observed in T rats. The resting bradycardia after exercise training is more likely to be dependent on alterations of the pacemaker cells, inasmuch as the intrinsic HR was markedly reduced.

Animals↗

PubMed1991

Platelet aggregation in allergic reactions.

The platelet aggregation in the presence of 4 aggregation inducers was studied in 63 allergic patients, consisting of atopic and non-atopic asthmatics and aspirin-sensitive subjects, before and after inhalation tests or in vitro incubation with allergen. Basal platelet aggregation was decreased in 43% of the atopic patients for adrenaline and also in a smaller percentage for other agonists. A decreased aggregation was also observed in 3 out of 6 nonatopic patients and in aspirin-sensitive patients. In vivo or in vitro provocation tests decreased aggregation in some additional patients. These results point out to a compromise of platelets in allergic mechanisms.

Humans↗

PubMed1991

Cellular interactions in asthma.

Immediate phase of asthma is induced by mast cells. Late phase asthmatic response is related to other cells such as, macrophages, lymphocytes, eosinophils, and could pass to chronicity and is usually associated with bronchial hyperreactivity. Pathological or functional studies of the different cells involved, could be done in peripheral blood, broncho-alveolar lavage, bronchial biopsies or nasal lavages.

Asthma↗

PubMed1991

T cells, macrophages and platelets in asthma.

The role of T cells, macrophages and platelets in asthma is discussed. Peripheric T cell populations are normal as well in atopic as in non atopic. Macrophages can release histamine releasing factors and PAF in presence of allergens. Platelets stimulated by contact with allergens or PAF decreased the aggregation pattern induced by common inducers. These data show that different cells can play a role in the inflammatory process in asthma.

Asthma↗

PubMed1989

[Platelet aggregation in asthma].

Platelet activation is one of the aspects of cellular interaction causing inflammation in asthma. Platelet aggregation has been studied in asthmatic patients in presence of different aggregation inducers (epinephrine, ADP, arachidonic acid). In 20 to 40% of the atopic asthmatic patients depending on the inducer and in some patients with non atopic asthma or aspirin sensitivity and asthma platelet aggregation is decreased. Bronchial provocation tests have not decreased platelet aggregation except in few cases. In vitro incubation of platelets with allergen extract has provoked an hypoaggregation mainly when incubation time or allergen concentration were increased. Platelets seem to play an important role in the inflammatory component of bronchial asthma.

Adenosine Diphosphate↗

PubMedDate not supplied

[Epidemiologic survey with histoplasmin and paracoccidioidine in Arapiraca-Alagoas].

Paracoccidioidin and histoplasmin intradermic tests were performed in 107 inhabitants in Arapiraca, Alagoas. The epidemiological survey was performed in both sexes and the ages varied from 2 to 71 years. Positive results with paracoccidioidin test were recorded in 11% and the histoplasmin test was positive in 14%. With the positivity of paracoccidioidin in the histoplasmin positive population the result shows a percentage of 33.33%, while with the positivity of histoplasmin in the paracoccidioidin positive population was 41%.

Adolescent↗

PubMedDate not supplied

Platelet reactivity to "in vitro" allergen challenge in asthmatic patients.

Platelet involvement in inflammation and allergic states is now well documented. In fact, it has been suggested that platelets can be triggered by either activated cells as monocytes and macrophages or by allergen itself. This latter possibility is still a matter of controversy. In this study we analysed platelet "in vitro" response to allergen, by optical aggregation technique, in 25 asthmatic patients, being 20 atopic and 5 non atopic patients. Platelet aggregation response to epinephrine, ADP, collagen and arachidonic acid was studied in all patients. In addition, allergen was added to platelet rich plasma and platelet reactivity was recorded both before and after stimulations with collagen. Platelet aggregation studies confirmed and abnormality of ADP induced platelet aggregation, that exhibited great variability among patients. In most cases this defect was the only one found in asthmatic patients and it should be further analysed. Results also showed a nonspecific response to allergen when dissolved in glycerol. This was due to glycerol rather than to allergen, since lyophilized allergen did not affect platelets, and glycerol added to platelet rich plasma induced the same type of curve. So, allergen by itself does not imply platelet aggregation. Experiments with IgE did not provoke either platelet agglutination or platelet aggregation. Furthermore, previous incubation with allergen immediately before collagen induced aggregation did not significantly change platelet response. This study allows the conclusion that platelet reactivity to allergen contact must be an expression of multicellular cooperation rather than a direct effect on platelet IgE receptors stimulation.

Adenosine Diphosphate↗