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Official Journal of the Italian Society of Thoracic Endoscopy
Indexed/Abstracted in: EMBASE, Scopus
Rubini A. 1, Porzionato A. 2, Salami E. 1, Macchi V. 2, Bosco G. 1
1 Department of Biomedical Sciences, Section Physiology, University of Padua, Padua, Italy;
2 Department of Molecular Medicine, Section Anatomy, University of Padua, Padua, Italy
AIM: Chronic amiodarone therapy may induce pulmonary toxicity, but the effects of acute administration on respiratory mechanics are unknown.
METHODS: We applied the end-inflation occlusion method in the rat to study the possible acute effects of amiodarone on respiratory mechanics and the related inspiratory work of breathing. Respiratory system hysteresis, an index of alveolar surfactant activity, and lung histology, were also investigated.
RESULTS: We found that amiodarone acutely increased both respiratory resistance components, i.e. the airway “ohmic”, and the additional visco-elastic, stress relaxation-linked, resistance. As expected, significant increments of the related “ohmic” and visco-elastic work of breathing were observed, together with an almost significant increment of the total work of breathing, while the elastic component remained unchanged. Respiratory system elastance and hysteresis, and lung histology, did not change significantly.
CONCLUSION: Our results indicate that, at variance with chronic administration, acute amiodarone does not affect alveolar surfactant activity nor lung histology, hence the elastic respiratory system properties, while its effects on respiratory system resistance suggest it should be cautiously utilised in obstructive lung diseases.