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Official Journal of the Italian Society of Thoracic Endoscopy
Indexed/Abstracted in: EMBASE, Scopus
Online ISSN 1827-1723
Section of Physiology, Department of Biomedical Sciences, University of Padua, Padua, Italy
The effects of some drugs of cardiovascular interest on respiratory mechanics which are described in the literature are reviewed, with particular attention to recently published results obtained by the end-inflation method on the rat. A description of this method is reported, which introduced the possibility to measure, together with the “ohmic” airway resistance and the respiratory system elastance, the additional “visco-elastic” resistance due to stress-relaxation. The latter represents a complex phenomenon most biological tissues exhibit, including respiratory system tissues: due to their visco-elastic properties, the tissues do not maintain constant stress under constant deformation, but slowly relax to a lower value. In the respiratory system, the visco-elastic pressure dissipation is responsible of a great amount of the total pressure that the inspiratory muscles have to develop to inflate the lungs. Recent data from the literature indicate that: 1) angiotensin-converting enzyme (ACE ) inhibition (captopril) causes a reduction of both the “ohmic” and the “visco-elastic” respiratory system resistances, leaving unaltered elastance; 2) amiodarone acutely increases both the “ohmic” and “visco-elastic” resistances, again leaving unaltered elastance; 3) nifedipine decreases the “ohmic” resistance and the elastance, while no significant effects were reported on the “visco-elastic” resistance. Drugs of cardiovascular interest often exhibit interesting effects on respiratory mechanics. Possible implications for the clinical usage of these drugs are suggested.