Airway anesthesia alone does not explain attenuation of histamine-induced bronchospasm by local anesthetics - A comparison of lidocaine, ropivacaine,and dyclonine

Citation
H. Groeben et al., Airway anesthesia alone does not explain attenuation of histamine-induced bronchospasm by local anesthetics - A comparison of lidocaine, ropivacaine,and dyclonine, ANESTHESIOL, 94(3), 2001, pp. 423-428
Citations number
28
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
00033022 → ACNP
Volume
94
Issue
3
Year of publication
2001
Pages
423 - 428
Database
ISI
SICI code
0003-3022(200103)94:3<423:AAADNE>2.0.ZU;2-9
Abstract
Background: Lidocaine inhalation attenuates histamine-induced bronchospasm while evoking airway anesthesia. Because this occurs at plasma concentratio ns much lower than those required for intravenous lidocaine to attenuate br onchial reactivity, this effect is likely related to topical airway anesthe sia and presumably independent of the specific local anesthetic used. There fore, the authors tested the effect of dyclonine, lidocaine, and ropivacain e inhalation on histamine-induced bronchospasm in 15 volunteers with. bronc hial hyperreactivity. Methods: Bronchial hyperreactivity was verified by an inhalational histamin e challenge. Histamine challenge was repeated after inhalation of dyclonine , lidocaine, ropivacaine, or placebo on 4 different days in a randomized, d ouble-blind fashion. Lung function, bronchial hyperreactivity to histamine, duration of local anesthesia, and lidocaine and ropivacaine plasma concent rations were measured. Statistical analyses were performed with the Friedma n and Wilcoxon rank tests. Data are presented as mean +/- SD. Results: The inhaled histamine concentration necessary for a 20% decrease o f forced expiratory volume in 1 s (PC20) was 7.0 +/- 5.0 mg/ml at the scree ning evaluation. Lidocaine and ropivacaine inhalation increased PC20 signif icantly to 16.1 +/- 12.9 and 16.5 +/- 13.6 mg/ml (P = 0.007), whereas inhal ation of dyclonine and saline did not (9.1 +/- 8.4 and 6.1 +/- 5.0 mg/ml, P = 0.7268). Furthermore, in contrast to saline and lidocaine, inhalation of both ropivacaine and dyclonine significantly decreased forced expiratory v olume in 1 s from baseline (P = 0.0016 and 0.0018, respectively). The longe st lasting and most intense anesthesia developed after dyclonine inhalation (48 +/- 13 vs. 28 +/- 8 [lidocaine] and 25 +/- 4 min [ropivacaine]). Conclusion: Both lidocaine and the new amide local anesthetic ropivacaine s ignificantly attenuate histamine-induced bronchospasm. In contrast, dycloni ne, despite its longer lasting and more intense local anesthesia, does not alter histamine-evoked bronchoconstriction and irritates the airways. Thus, airway anesthesia alone does not necessarily attenuate bronchial hyperreac tivity. Other properties of inhaled local anesthetics may be responsible fo r attenuation of bronchial hyperreactivity.