Effects of pulmonary vascular pressures and flow on airway and parenchymal mechanics in isolated rat lungs

Author:

Peták Ferenc1,Habre Walid2,Hantos Zoltán3,Sly Peter D.4,Morel Denis R.1

Affiliation:

1. Division of Anesthesiologic Investigations, University of Geneva, 1211 Geneva;

2. Division of Anesthesia, Geneva Children's Hospital, 1205 Geneva, Switzerland;

3. Department of Medical Informatics and Engineering, University of Szeged, Szeged 6720, Hungary; and

4. Division of Clinical Sciences, Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth 6008, Australia

Abstract

Changes in pulmonary hemodynamics have been shown to alter the mechanical properties of the lungs, but the exact mechanisms are not clear. We therefore investigated the effects of alterations in pulmonary vascular pressure and flow (Q˙p) on the mechanical properties of the airways and the parenchyma by varying these parameters independently in three groups of isolated perfused normal rat lungs. The pulmonary capillary pressure (Pcest), estimated from the pulmonary arterial (Ppa) and left atrial pressure (Pla), was increased at constant Q˙p ( n = 7), orQ˙p was changed at Pcest = 10 mmHg ( n = 7) and at Pcest = 20 mmHg ( n = 6). In each condition, the airway resistance (Raw) and parenchymal damping (G) and elastance (H) were identified from the low-frequency pulmonary input impedance spectra. The results of measurements made under isogravimetric conditions were analyzed. The changes observed in the mechanical parameters were consistent with an altered Pla: monotonous increases in Raw were observed with increasing Pla, whereas G and H were minimal at Pla of ∼7–10 mmHg and increased at lower and higher Pla. The results indicate that Pla, and not Ppa or Q˙p, is the primary determinant of the mechanical condition of the lungs after acute changes in pulmonary hemodynamics: the parenchymal mechanics are impaired if Pla is lower or higher than physiological, whereas airway narrowing occurs at high Pla.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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