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Biomedical subjects

G A Wassink

Publications and source records attributed to G A Wassink.

11 recordsLinked to original sources
PubMed1987

Changes in the broncho-alveolar lavage fluid in smokers and patients with chronic obstructive lung disease.

Direct contact of the cells normally present in the bronchial lumen, such as alveolar macrophages, with air pollutants (e.g. cigarette smoke) can lead to the activation of these cells. This activation is beneficial for the cleaning task these cells have in the bronchial tree, but also leads to the release of chemotactic substances, toxic oxygen radicals, enzymes and mediators responsible for bronchial obstruction. As a first step in these processes, an enhanced chemotactic activity can attract neutrophils to the bronchial lumen, where they help by cleaning the lungs from possible dangerous intruders, but can also cause damage to the normal lung architecture. In the present study concerned with the pathogenesis of chronic obstructive lung disease (COLD), broncho-alveolar lavage (BAL) was performed in 35 individuals, who could be divided on he basis of their history and lung function into normal/nonsmokers, normal/smokers, COLD-patients/nonsmokers and COLD-patients/smokers. Neutrophilic chemotactic activity was assayed using Boyden chambers where the patients' own neutrophils were tested. More neutrophils and more neutrophilic chemotactic activity were found in the BAL-fluid of the smokers and COLD-patients. A correlation was demonstrated between the amount of chemotactic activity released during the incubation of cells obtained by BAL and the airway resistance or the airway conductance. These data suggest an enhanced chemotactic activity as one of the initiating factors in the pathogenesis of chronic obstructive lung disease.

Bronchoalveolar Lavage Fluid↗
PubMed1987

Changes in alveolar macrophage enzyme content and activity in smokers and patients with chronic obstructive lung disease.

An influx of polymorphonuclear and mononuclear cells into the lungs of smokers and patients with chronic obstructive lung disease (COLD) is thought to be an important factor in the development of pulmonary emphysema. Next to the synthesis and release of toxic oxygen radicals and mediators, an enhanced production and activity of proteolytic enzymes could play an important role in the pathogenesis of emphysema. In the present study changes were investigated in the broncho-alveolar lavage (BAL) fluid and BAL-cells, especially in alveolar macrophages. Pulmonary lavages were performed in the middle lobe with sterile saline of 37 degrees C in individuals, who could be divided on the basis of their history and lung function into normal/nonsmokers, normal/smokers, COLD-patients/nonsmokers and COLD-patients/smokers. Alveolar macrophages obtained by BAL were stained for different lysosomal enzymes. Isolated BAL-fluid and BAL-cells were assayed for elastolytic activity. In alveolar macrophages of smoking COLD-patients significantly more beta-glucuronidase could be demonstrated. Elastolytic activity changed with smoking habits, suggesting an enhanced release of elastolytic enzymes. No correlation was found between elastolytic activity and the amount of polymorphonuclear cells in the BAL-fluid. From these results it may be concluded that enzymes from alveolar macrophages play a more important role in the pathogenesis of emphysema than those from polymorphonuclear cells.

Female↗
PubMed1984

Specific leukotriene formation by purified human eosinophils and neutrophils.

Human granulocytes isolated from peripheral blood have been described to synthesize both LTB4 and LTC4 from arachidonic acid. We have observed that the amount of LTC4 produced by human granulocyte preparations is strongly dependent on the relative amount of eosinophils. To investigate a possibly significant difference in leukotriene synthesis of the eosinophilic and neutrophilic granulocytes, we developed a purification method to isolate both cell types from granulocytes obtained from the blood of healthy donors. Leukotrienes were generated by incubation of the purified cells with arachidonic acid, calcium ionophore A23187, calcium-chloride and reduced glutathione. Surprisingly, eosinophils were found to produce almost exclusively the spasmogenic LTC4. In contrast, neutrophils produce almost exclusively the chemotactic LTB4, its omega-hydroxylated metabolite 20-hydroxy-LTB4 and two non-enzymically formed LTB4 isomers.

Arachidonic Acid↗
PubMed1984

Adrenoceptors in lung tissue: characterization, modulation and relations with pulmonary function.

Adrenoceptor (sub)populations (alpha 1, beta and beta 1/beta 2 ratio) in human lung tissue were characterized by means of radioligand binding assays. Lung tissue specimens for these assays were obtained at thoracotomy from normal individuals and COLD patients. The patients were not receiving therapy known to influence adrenoceptor characteristics. In COLD patients, the number of alpha 1-adrenoceptors appeared to be markedly enhanced while the relative amount of beta 2-adrenoceptors was decreased. Furthermore, some adrenoceptors seemed to be correlated to pulmonary function both in the normal individuals and COLD patients. In-vitro modulation with disodium cromoglycate and ketotifen revealed therapeutic possibilities for these substances based on other pharmacological mechanisms than hitherto assumed.

Cromolyn Sodium↗
PubMed1983

Relevance of changes in adrenoceptor characteristics after terbutaline treatment.

Rats were treated with terbutaline in order to specify the in vivo effects of beta 2-sympathicomimetic treatment in relation with desensitization phenomena on the level of pulmonary adrenoceptors. Maximal binding of 3H-dihydroalprenolol (3H-DHA) to lung membrane preparations, binding affinity and the relative amount of beta 2-adrenoceptors were used as parameters. These were established 1, 3, and 6 days after a 10 days terbutaline treatment and compared with control values. Ten days treatment did not cause significant changes in the parameters measured. However, maximal binding was enhanced 3 and 6 days after the last treatment, binding affinity was enhanced 3 days after the last treatment, while the relative amount of beta 2-adrenoceptors was diminished 1 and 6 days after termination of the treatment. When the amount of beta 2-adrenoceptors was calculated in terms of 3H-DHA binding, an increase could be shown 3 days after the last terbutaline treatment. Therefore the direct influence of the treatment on the beta-adrenoceptor population appeared to be small, dependent on the parameter used and probably not eliciting a functional desensitization.

Animals↗