[Effect of progesterone on experimental pulmonary emphysema].
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Biomedical subjects
Publications and source records attributed to M Szmidt.
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Twenty-nine patients with asthma and aspirin-sensitivity were studied in an attempt to induce tolerance to aspirin (ASA). Starting with the smallest ASA doses eliciting bronchial obstruction (threshold doses) we doubled the doses on subsequent days and finally achieved good tolerance of 600 mg ASA per day in 27 patients. It was more difficult to achieve tolerance in patients with low ASA-thresholds than in patients with high ones. Daily ASA administration led to prolongation of the refractory state but when the intervals between consecutive doses were increased, aspirin hypersensitivity recurred. The pause sufficient for a recurrence of sensitivity to ASA was measured in 16 patients and ranged from 24 h to 9 days. Twelve patients challenged with indomethacin after ASA-desensitisation showed good drug tolerance.
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The influence of acetylsalicylic acid (ASA) on skin response to intradermal injection of compound 48/80 and histamine was studied in order to determine whether ASA elicits any abnormalities also in the skin of asthmatics reacting with bronchoconstriction to ingestion of this drug. The applied ASA dose (mean dose 150 mg) elicited bronchoconstriction in all 16 patients with asthma and ASA sensitivity (mean fall of FEV1 34%) and increased the weal response to compound 48/80 to about 51% (P less than 0.05) as compared with the response before the ASA-challenge. In asthmatic persons without ASA sensitivity a 150 mg ASA dose did not influence the skin response to any of the reagents. On the other hand, a 600 mg dose decreased skin response to histamine and compound 48/80 in persons without ASA intolerance, although the decrease was statistically significant only in the flare after compound 48/80 (P less than 0.05). The authors believe that additional local defect is needed to reveal sensitivity to ASA in the skin of ASA-sensitive asthmatics, just as bronchial hyperreactivity is indispensible for revealing the action of ASA in the bronchi.
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Bronchial challenge with polymyxin B caused a significant bronchoconstriction in 85% of atopic asthmatics. In all atopic asthmatics in whom inhalation of polymyxin B elicited bronchoconstriction, a significant, although not always parallel to the grade of bronchoconstriction, increase in histaminemia was observed. If bronchoconstriction was not elicited, the increase in histaminemia did not occur. It constitutes evidence that the bronchoconstricting effect of polymyxin B is exclusively due to degranulation of mast cells and that histamine released in the bronchi can increase the concentration of histamine in the blood.
To determine the role of mast cells in aspirin-induced bronchoconstriction, venous histaminemia was measured in 17 aspirin-sensitive patients before and after administration of aspirin. Ventilatory disturbances were measured spirographically. Venous histaminemia was determined according to Lorenz. In 11 patients the mean increase of histaminemia was from 39.6 ng/ml to 107.0 ng/ml. In the remaining 6 patients no change in histaminemia was observed after the challenge. In patients exhibiting the increase of histaminemia, symptoms of hypersensitivity to aspirin, other than dyspnea, were not common and stronger. The authors discuss a possible relationship of the aspirin effect, disturbances in prostaglandin synthesis and histamine release.
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