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Blood concentration of endogenous beta-endorphines can change during the clinical evolution of chronic bronchopneumopathies. The authors assessed the beta-endorphine concentrations in the pulmonary arterial and systemic arterial blood in 8 asthmatic patients during a symptom-free period and after methacholine-induced bronchospasm. The beta-endorphine analysis was performed in duplicate dor each sample, by means of a RIA assay. There is not difference in the systemic arterial blood concentration of beta-endorphines between asthmatic patients and normal subjects. Furthermore, there is no change in the beta-endorphine blood concentration during the passage through the pulmonary tissue after methacoline-induced bronchospasm.

We present a case of severe intraoperative bronchospasm and laryngospasm, that happened after the administration of atracurium 0.5 mg/kg-1; this episode was very difficult to manage, in spite of a prompt bronchodilative treatment. This episode of bronchospasm happened again after extubation and it was so severe that it was necessary to intubate the patient quickly again. We administered bronchodilatative drugs again, and after half an hour it was possible to extubate the patient and to send him to the ward. He had no problems in the postoperative period. We carried on some investigations to evaluate the nature of this reaction: we measured the level of IgE, C3 and C4 complement factor during operation (one sample), in the first and second postoperative days. Moreover we did an intradermal test for all the drugs used during the operation. We concluded that it was an anaphylactoid reaction, sustained by atracurium.

Since their introduction in clinical practice beta-blocker drugs are known to be able to induce bronchospasm. However, this adverse effect may develop only in subjects with asthma, chronic bronchitis and/or airways hyper-reactivity. Although this potentially adverse effect of beta-blockers on the airways has long been recognized, its mechanism in inducing bronchospasm remains unclear. The Authors report a case of severe bronchoconstrictive episodes with respiratory failure following the administration of a timolol ophthalmic solution in a 51 yr old woman. Pharmacokinetics, preventive and therapeutic aspects of timolol eyedrop-induced bronchospasm are discussed.

Bronchial release appears to be regulated by the nonadrenergic noncholinergic system whose transmitter is very probably VIP. In vivo and in vitro studies were conducted to discover whether peptide modifies basic function and/or bronchial spasm provoked by histamine. The data collected show that VIP failed to cause bronchodilation but protects against histamine induced bronchoconstriction both in vivo and in vitro.

A new beta 2-agonists, broxaterol, administered by oral spray has been tested to evaluate its action modifying on the bronchial hyperreactivity to metacholine. Such drug has been administered double blind Vs salbutamol individualizing for both, at 15' and 90' premedication the PD20 FEV1 (doses of metacholine necessary to reduce of 20% the FEV1). The results that we have obtained confirm the protective capacity for both drugs on the bronchoconstriction induced by aspecific stimulus. However, in confront with salbutamol, the broxaterol presents an action more lasting in the time. Such requisite and absence of collateral effects permit to affirm that this new beta 2-agonists is fit for its utilization in the infantile intrinsic asthma.