Impact of microvascular circulation on peripheral lung stability

Abstract

volvement of pulmonary circulation in the mechanical properties was studied in isolated rat lungs. Pulmonary input impedance (ZL) was measured at a mean transpulmonary pressure (Ptp mean) of 2 cmH2O before and after physiological perfusion with either blood or albumin. In these lungs and in a group of unperfused lungs, ZL was also measured at Ptp mean values between 1 and 8 cmH2O. Airway resistance (R aw) and parenchymal damping (G) and elastance (H) were estimated from ZL. End-expiratory lung volume (EELV) was measured by immersion before and after blood perfusion. The orientation of the elastin fibers relative to the basal membrane was assessed in additional unperfused and blood-perfused lungs. Pressurization of the pulmonary capillaries significantly decreased H by 31.5 Ϯ 3.7% and 18.7 Ϯ 2.7% for blood and albumin, respectively. Perfusion had no effect on R aw but markedly altered the Ptpmean dependences of G and H Ͻ4 cmH 2O, with significantly lower values than in the unperfused lungs. At a Ptp mean of 2 cmH2O, EELV increased by 31 Ϯ 11% (P ϭ 0.01) following pressurization of the capillaries, and the elastin fibers became more parallel to the basal membrane. Because the organization of elastin fibers results in smaller H values of the individual alveolus, the higher H in the unperfused lungs is probably due to a partial alveolar collapse leading to a loss in lung volume. We conclude that the physiological pressure in the pulmonary capillaries is an important mechanical factor in the maintenance of the stability of the alveolar architecture. forced oscillations; alveolar wall; elastin; end-expiratory lung volume THE MECHANICAL PROPERTIES of the lungs are significantly influenced by changes in the pulmonary hemodynamic conditions (3,7,9,11,20,21, 27,29,(35)(36)(37)40). Numerous clinical (3,7,9,11,20, 27) and experimental studies (29,36,37) have demonstrated that elevation of the pulmonary blood flow (7,20, 27) and/or pressure (3, 11, 29, 36, 37) leads to a deterioration of the lung function via a decrease in functional residual capacity (FRC) (7) and/or stiffening of the alveolar wall (40). Although the qualitative examinations performed by von Basch (38a) in 1889 suggested that not only congestion, but also pulmonary hypoperfusion, can alter the lung configuration, few data are available concerning the changes in the mechanical conditions of the lungs during hypoperfusion or the complete absence of pulmonary perfusion (21,25,29,35). Mitzner et al. (25) observed a transient increase in the respiratory resistance and a decrease in the compliance after occluding a pulmonary artery in mice, but the explanation of this finding remained unclarified. Furthermore, we recently demonstrated that low pulmonary venous pressures cause an impairment in lung mechanics, manifested in increases in the parenchymal resistive and elastic parameters, while the airway properties remain unaffected (29). However, the mechanisms responsible for the compromised lung mechanics at low vascular pressure or when there is no perfusion ...

Interactions between pulmonary hemodynamics and lung mechanics

“…These findings suggest that the loss of alveolar stability due to the decreased level of capillary filling not only has an acute effect [2], but also precipitates the potentially increased surface tension, and histological injuries [44] are not likely to play a role in the parenchymal mechanical deterioration observed in the present study, where the aim was the investigation of various Pc levels during relatively short ventilation times.…”

“…This phenomenon has been shown to be of greater importance in situations when the lung volume is lowered to below the closing volume [2].…”

“…It has been also demonstrated that, at low vascular pressure, the lung mechanics is compromised by loss of the mechanical tethering effect exerted by the pressurized pulmonary capillary network [2]. These results led to the conclusion that physiological pressure in the pulmonary capillaries is an important mechanical factor for the maintenance of the stability of the alveolar architecture.…”

“…This unity of conducting airways terminating in the alveoli and the pulmonary capillaries forms a complex system where any change in one compartment affect the other via cardiopulmonary interactions. This mechanical interdependence is manifested in airway and/or lung tissue changes subsequent to acute or chronic alterations in the pulmonary hemodynamics [1,2].…”

“…There is increasing evidence that not only lung congestion, but also hypoperfusion in the pulmonary circulation causes impairments in lung mechanics [1, 2,[9][10][11]. It has been also demonstrated that, at low vascular pressure, the lung mechanics is compromised by loss of the mechanical tethering effect exerted by the pressurized pulmonary capillary network [2].…”