title: The contribution of the pulmonary microvascular pressure in the maintenance of an open lung during mechanical ventilation.
abstract: Changes in pulmonary hemodynamics modify the mechanical properties of the lungs. The effects of alterations in pulmonary capillary pressure (Pc) were investigated on the airway and lung tissue mechanics during positive-pressure ventilation and following lung recruitment maneuvers. Isolated, mechanically normoventilated (PEEP 2.5 cmH(2)O) rat lungs were perfused with Pc set to 0 (unperfused), 5, 10 or 15 mmHg, in random sequence. The pulmonary input impedance (ZL) was measured at end-expiration before and after a 10-min long ventilation. After inflation of the lung to 30 cmH(2)O during P-V curve recordings, another set of ZL was measured to evaluate the degree of recruitment. The PEEP was then decreased to 0.5 cmH(2)O and the sequence was repeated. Airway resistance and parenchymal damping and elastance (H) were estimated from ZL by model fitting. From the P-V curves, elastance (E) and hysteresis indices were determined. Mechanical ventilation at both PEEP levels resulted primarily in elevations in the tissue parameters, with the greatest increases at the 0 Pc level (H changes of 27.8+/-4.2 and 61.3+/-3.7% at 2.5 and 0.5 cmH(2)O PEEP, respectively). The maintenance of physiological Pc (10 mmHg) led to a significantly lower elevation in H (11.6+/-1.5% versus 31.4+/-3.6%). The changes in the oscillatory mechanics were also reflected in E and the hysteresis of the P-V curves. These findings indicate that pulmonary hypoperfusion during mechanical ventilation forecasts a parenchymal mechanical deterioration. Physiological pressure in the pulmonary capillaries is therefore an important mechanical factor promoting maintenance of the stability of the alveolar architecture during positive-pressure mechanical ventilation.
authors.affiliation: Anesthesiological Investigations Unit, University Hospitals of Geneva, Geneva, Switzerland.
authors.forename: Gergely
authors.initials: G
authors.lastname: Albu
authors.forename: Walid
authors.initials: W
authors.lastname: Habre
authors.forename: Fabienne
authors.initials: F
authors.lastname: Fontao
authors.forename: Denis R
authors.initials: DR
authors.lastname: Morel
authors.forename: Ferenc
authors.initials: F
authors.lastname: Petak
mesh_terms: D000403:Airway Resistance / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D008168:Lung / Q000166:cytology* / Q000502:physiology*; D008297:Male; D010477:Perfusion; D011650:Pulmonary Alveoli / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000379:methods*; D015656:Respiratory Mechanics / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology