Whither beta-adrenergic tachyphylaxis?
1982; Elsevier BV; Volume: 70; Issue: 6 Linguagem: Inglês
10.1016/0091-6749(82)90002-1
ISSN1097-6825
Autores Tópico(s)Inhalation and Respiratory Drug Delivery
Resumoat the outset, or no longer has any regard for his professional reputation. The writer fears that he is guilty of all three, and hence is easily trapped into this assignment. The question of tachyphylaxis arose as a result of a rise in asthma deaths in the United Kingdom in the 6Os, which paralleled the appearance on the market of a metered dose inhaler delivering large doses of isoproterenol.’ Coincident with the manufacturer’s reduction in dose/puff and warnings against overuse was a subsidence in this excess of deaths, leading many to conclude that the two may have been related through the phenomenon of tachyphylaxis. Myocardial toxicity from the combination of isoproterenol, freon propellents, and hypoxemia was also considered. Delay in treatment after initial effectiveness of the new inhaler was perhaps the principal cause. The subsidence in mortality also coincided with the introduction of better management of asthma and particularly the introduction of corticosteroids and cromolyn sodium, so that the descending limb of this epidemic of deaths cannot necessarily be invoked in support of the isoproterenol association. In spite of steadily increasing sales of specific beta,-aerosol inhalers since 1969, death rates remained stable .2 There also seemed to be good evidence that isoproterenol used excessively can be responsible for insensitivity of the bronchial beta receptors in certain individuals, leading to worsening of their asthma,3 while a few individuals had adverse reactions to usual doses.* With the introduction of oral beta, agonists, the issue of tachyphylaxis rose again, with evidence
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