Airway mechanics and lung tissue viscoelasticity: effects of altered blood hematocrit in the pulmonary circulation.
The contribution of the hematocrit (Hct) of the blood in the pulmonary vasculature to the overall lung mechanics has not been characterized. We therefore set out to establish how changes of the Hct level in the pulmonary circulation affect the airway and lung tissue viscoelastic properties. The Hct level of the blood in an isolated perfused rat lung model was randomly altered. Intermediate (26.5%), followed by low (6.6%) or normal (43.7%), Hct was set in two consecutive sequences. The pulmonary capillary pressure was maintained constant throughout the experiment, and the pulmonary hemodynamic parameters were monitored continuously. The airway resistance (Raw), the viscous (G) and elastic (H) parameters, and the hysteresivity (η = G/H) of the lung tissues were obtained from measurements of forced oscillatory input impedance data. Raw was not affected by the alterations of the Hct levels. As concerns the lung tissues, the decrease of Hct to intermediate or low levels resulted in close to proportional decreases in the viscoelastic parameters G [16.5 ± 7.7% (SD), 12.1 ± 9.5%, P < 0.005] and H (13.2 ± 8.6%, 10.8 ± 4.7%, P < 0.001). No significant changes in η were detected in a wide range of Hct, which indicates that coupled processes cause alterations in the resistive and elastic properties of the lungs following Hct changes in the pulmonary circulation. The diminishment of the viscous and elastic parameters of the pulmonary parenchyma following a reduction of blood Hct demonstrates the significant contribution of the red blood cells to the overall lung viscoelasticity.
Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary; petak.ferenc@med.u-szeged.hu.
Ferenc
F
Peták
Department of Medical Physics and Informatics, University of Szeged, Szeged, Hungary;
Gergely H
GH
Fodor
Department of Anesthesiology and Intensive Therapy, University of Szeged, Szeged, Hungary;
Barna
B
Babik
Pathophysiological Experimental Platform, Department of Anesthesiology, Pharmacology and Intensive Care, University of Geneva, Geneva, Switzerland; and Pediatric Anesthesia Unit, Geneva Children's Hospital, Geneva, Switzerland.
Walid
W
Habre
D000403:Airway Resistance / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004548:Elasticity / Q000502:physiology*; D006400:Hematocrit / Q000379:methods; D006439:Hemodynamics / Q000502:physiology; D008168:Lung / Q000502:physiology*; D008297:Male; D011652:Pulmonary Circulation / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D014783:Viscosity
cardiopulmonary interactions; lung mechanics; lung tissue elastance; lung tissue resistance; pulmonary vasculature