We investigated whether fatigue of the expiratory muscle, that is, the abdominal muscle, may account for a change in the respiratory effort sensation in normal subjects during expiratory threshold loading. The respiratory effort sensation was scored using a modified Borg scale. Expiratory muscle fatigue was assessed both from changes in the maximal static expiratory pressure and in the centroid frequency (fc) of the abdominal muscle electromyogram (EMG). Expiratory threshold loading (magnitude of threshold; 40 to 60% of the maximal expiratory pressure at FRC, breathing frequency = 15/min, and duty cycle = 0.5) was continued until exhaustion or for 30 min. Loading was repeated following a 15-min recovery period after the end of the first expiratory loading. The maximal static expiratory pressure during loading (Pmmax) decreased initially and then remained decreased. Decreases were smaller with the 40% load (22 +/- 6%, SEM) than with the 60% load (37 +/- 3%) (p less than 0.05). The decrease during the second run of the 60% load was greater than during the first (p less than 0.01 by ANOVA). The maximal expiratory pressure at TLC before the second run of the 60% load was decreased by 9 +/- 3% compared with the control (p less than 0.02) but that with the 40% load was not. The fc with the 60% load decreased initially by 8 +/- 1% and then remained constant, although no change was observed with the 40% load.(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate how pulmonary surfactant influences alveolar structure in vivo, we examined the alveolar surface area-to-lung volume (S/V) ratio of the lung parenchyma of a live dog by light-scattering stereology before and after saline lavage. We measured the backscattered light pattern produced by applying a laser beam to the pleural surface of a ventilated animal and obtained the S/V [equivalent to the inverse of the optical mean free path (lambda)]. After saline lavage, V at transpulmonary pressure (P) of 30 cmH2O (defined as total lung capacity) decreased by 11.1 +/- 3.1% (SD) and the P-V curve shifted to a lower V. The lambda-V curve was shifted to a higher lambda and to a lower V after saline lavage. S/V decreased after saline lavage (lambda increased by 38 +/- 27% on the deflation limb at a V of 80% of control total lung capacity). The alveolar surface tension increased after saline lavage, and the increase in surface tension was greater on inflation than on deflation. We conclude that depletion of pulmonary surfactant increases the alveolar surface tension in vivo, resulting in a decrease in S/V.
It is unknown how the in vivo alveolar surface area-to-volume ratio (S/V) changes in low-pressure pulmonary edema. Here, the S/V is the area of the air-tissue interface per unit total volume (air plus tissue). We hypothesized that in oleic acid (OA)-induced edema inactivation of the pulmonary surfactant may increase surface tension and decrease the S/V at any given lung volume. OA (0.04 mg/kg) was intravenously injected into dogs. We measured the in vivo S/V (equivalent to the inverse of optical mean free path by light-scattering stereology and the pressure-volume (PV) curve 60-90 min after OA administration. OA administration decreased the lung volume at each transpulmonary pressure and increased the wet-to-dry weight ratio. The S/V decreased after OA administration (optical mean free path increased). The air-filled PV curves shifted downward after OA, but the saline-filled PV curves after OA administration did not differ significantly from control saline-filled curves. The difference in transpulmonary pressure between air- and saline-filled PV curves (an index of the magnitude of surface tension) was increased in OA-induced pulmonary edema. This study suggests that in OA-induced pulmonary edema the alveolar surface tension increases and the S/V decreases, presumably due to inactivation of surfactant by serum leakage to alveoli.
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