Journal of applied physiology
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Positive end-expiratory pressure (PEEP), by increasing lung volume in acute lung injury, may recruit terminal air spaces in the involved regions, but may also distend noninvolved regions increasing extravascular lung water and worsening gas exchange. We investigated the effect of increasing levels of PEEP on arterial oxygenation in 26 anesthesized dogs with unilateral acid pneumonitis and studied the influences of gravity and distribution of the injury on this effect. Arterial PO2 was consistently higher when the noninjured lung was dependent than in the supine or injured lung-dependent positions. ⋯ However, 15 cmH2O PEEP resulted in worsening of gas exchange, increased dead space ventilation, and diminished static compliance. The adverse effects of high levels of PEEP on arterial oxygenation were similar whether the injured lung was dependent or not and were evident a lower levels of PEEP in one group of dogs in which the unilateral injury was more diffuse and in which the upper and middle lobes were also involved. Thus, the compressive effects of high levels of PEEP on alveolar capillaries in the noninjured lung are influenced by the extent and distribution of injury in the injured lung, but not by local forces governing regional blood flow distribution.
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In nine cats and nine human subjects anesthetized with alfaxalone, respiratory activity and tracheal pressure were recorded prior to and during occlusion of the airway at end inspiration or end expiration. Lung inflations at the end of expiration were also performed. In addition, the ventilatory pattern was analyzed during hypercapnia. ⋯ These results indicate that the Breuer-Hering reflex, which delays the onset of inspiration during inflation was equally operative in cats and humans. In contrast, the "Breuer-Hering threshold curve," which accounts for the off-switch" of inspiration was different in cats and humans. Thus, in summary, the Breuer-Hering inflation reflex is operative in human subjects, but it does not seem to be involved in the control of the inspiratory off-switch mechanism during increases respiratory activity resulting from hypercapnia.
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We tested the hypothesis that decreases in alveolar O2 pressure (PAO2) of a large lung compartment would, through decreases in arterial O2 pressure (PaO2) and mixed venous O2 pressure (PVO2), result in decreases in PAO2 of the remaining small lung compartment; thus large-compartment hypoxic pulmonary vasoconstriction (HPV) would be accompanied by concomitant small-compartment HPV. In eight pentobarbital-anesthetized dogs, whose left lower lobe (LLL) inspired oxygen concentration (FIO2) was constantly 0.21, selective stepwise reductions in the rest of the lung (RL) FIO2 from 1.0 to 0.15 caused the electromagnetically measured LLL blood flow (QLLL/Qt), pulmonary vascular resistance of RL (PVRRL), and PVRLLL to increase while RL PAO2, PaO2, PVO2, and LLL PAO2 progressively decreased. ⋯ Based on previously established PAO2 levels of maximum HPV gain and LLL dose-response curves, the RL FIO2-induced changes in QLLL/QT can be explained by different rates of change in RL and LLL PAO2 and PVR. Thus, our findings indicate that if decreases in RL FIO2 cause, in turn, large decreases in PaO2, PVO2 and "normoxic" lung PAO2, then PVO2 is an important determinant of the magnitude of the HPV response.
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Comparative Study
Extrapericardial and esophageal pressures with positive end-expiratory pressure in dogs.
Using flat balloon techniques to minimize distortion and artifacts, we studied the effect of positive end-expiratory pressure (PEEP) on local surface pressures between the lung and pericardium overlying the right (R) and left (L) ventricles of ventilated closed-chest anesthetized dogs in right lateral decubitus position. To test the hypothesis that local extrapericardial [Pep(L) and Pep(R)] and average pleural pressures change equally with PEEP, we also measured esophageal pressure (Pes). When 10-cmH2O PEEP was applied, mean increases in Pes, Pep(L), and Pep(R) were 6.2, 5.6, and 5.3 cmH2O, respectively. ⋯ At each level of PEEP, volume infusion was used to increase stroke volume. Volume infusion at 20-cmH2O PEEP was associated with small 1.0- and 1.5-cmH2O increases in Pep but no change in Pes. Analysis of confidence limits showed that application of up to 20-cmH2O PEEP, with or without volume infusion to restore stroke volume, is associated with nearly equal changes in esophageal and local extrapericardial pressures.
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Correlation between transcutaneous and arterial CO2 partial pressure (Ptcco2, and Paco2) under normal and hemorrhagic shock conditions was evaluated in rabbits. Under normal conditions the Paco2-to-Ptcco2 least-squares regression line had a slope of 1.03 an intercept of 4.57 Torr, and a root mean variance of +/- 3.79 Torr. Under hemorrhagic shock conditions the slope remained similar, but the intercept increased, producing a significant difference between arterial and transcutaneous values. ⋯ The transcutaneous response time (90%) under conditions produced by breathing 10% CO2 lagged 2.8 +/- 1.4 min behind that of the breathing 10% CO2 lagged 2.8 +/- 1.4 min behind that of the Paco2. The difference between transcutaneous and arterial CO2 observed during hemorrhagic shock and the lag in transcutaneous response time can be altered by topical application of dimethyl sulfoxide, by altering both flow and permeability. These results indicate that good Ptcco2-to-Paco2 correlation exists under normal conditions and that hemorrhagic shock will produce tissue CO2 accumulation and therefore higher than arterial Ptcco2 values.