Journal of applied physiology
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Comparative Study
Instantaneous venous return curves in an intact canine preparation.
The relationship between right atrial pressure (Pra) and venous return describes a venous return curve. Because changes in venous return and right ventricular stroke volume (SVRV) are similar during small tidal volume (VT) breathing, we compared the relationship of SVRV and Pra during positive-pressure ventilation (VT less than 10 ml/kg) in 17 pentobarbital-anesthetized, closed-chest, canine preparations. The SVRV-Pra relationship describes a straight line with a negative slope and a positive mean systemic pressure (Pms)-zero flow intercept (instantaneous Pms). ⋯ Vascular compliance determined by adding and removing blood from the intravascular space displays a curvilinear hysteresis. The instantaneous venous return curve is affected by intravascular blood volume, vasomotor tone, and resistance to venous return. The relationship between SVRV and Pra during small VT breathing define instantaneous venous return curves similar to those described using right-heart bypass preparations.
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Endotracheal intubation of the rat under direct vision is described together with the details of procedures and apparatus for conducting inhalation anesthesia in this species. Our intubation method requires no special manufacture of equipment, because it employs the human laryngoscope equipped with an infant blade (size 0). Using inhalation anesthetics such as enflurane or halothane for induction, clear laryngoscopic visualization of the glottis is reliably obtained, allowing rapid and routine intubation of the rat in a highly predictable amount of time. In contrast, the injected anesthetics such as ketamine or pentobarbital sodium seem unsuited to laryngoscopic intubation as a result of problems of variable induction times, copious oral secretions, and strong pharyngeal-laryngeal reflexes.
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Pressure-volume curves were obtained from excised left lungs of goats at 4, 24, and 48 h after tracheal instillation of 2.5 ml/kg of 0.1 N HCl. Air total lung capacity (TLC) at transpulmonary pressure (PL) = 35 cmH2O was 38.8 ml/kg body weight before acid, and was reduced sharply to 21.1 at 4 h, then increased to 25.6 at 24 h and 32.1 at 48 h. Excess extravascular lung water (EVLW) could account for only part of the volume reductions. ⋯ Air volume at a PL = 10 cmH2O on deflation fell from 82.0 to 72.1% TLC at 4 h, but was near control at 24 and 48 h. The reduction in ventilated volume was not reflected in proportionately increased shunt; therefore, some compensatory vasoconstriction must have occurred. We suggest that in affected regions increased surface forces, increased EVLW, and airway obstruction caused reductions of lung volume.
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Alveolar liquid pressure (Pliq) was measured by micropipettes in conjunction with a servo-nulling pressure measuring system in isolated air-inflated edematous dog lungs. Pliq was measured in lungs either washed with a detergent (0.01% Triton X-100) or subjected to refrigeration for 2-3 days followed by ventilation for 3 h. At 55% of total lung capacity (TLC, the volume at a transpulmonary pressure (Ptp) of 25 cmH2O before treatment), in both the Triton-washed and the ventilated lung, Ptp increased from 5 to 11 cmH2O, whereas Pliq, decreased from -3 to -11 cmH2O relative to alveolar air pressure. ⋯ Alveolar surface tension (T) was estimated from the Laplace equation for a spherical air-liquid interface, assuming that the radius of curvature varies as (volume)n, for -1/3 less than n less than 1/3. For uniform expansion of alveoli (n = 1/3), estimated T was 6 and 18 dyn/cm at 55 and 85% TLC, respectively, before treatment and increased to 23 and 40 dyn/cm following either Triton washing or ventilation. If pericapillary interstitial fluid pressure (Pi) equaled Pliq in edematous lungs, increases in T might reduce Pi and increase extravascular fluid accumulation in lungs made stiff by either Triton washing or cooling and ventilation using large tidal volumes.
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Comparative Study
Contribution of hypoventilation to sleep oxygen desaturation in chronic obstructive pulmonary disease.
The purpose of this study was to determine whether hypoventilation contributes to the sleep hypoxemia observed in chronic obstructive pulmonary disease (COPD) patients and to examine breathing pattern and respiratory muscle electromyographic (EMG) activity during these episodes. Seven COPD patients who experienced at least a 10% decrease in arterial O2 saturation (SaO2) during rapid-eye-movement sleep (REM) sleep, six COPD patients with a minimal fall in SaO2, and five healthy subjects were studied. An inductance vest was used to quantitate ventilation. ⋯ SaO2 followed the hypopneic and hyperpneic breathing in REM sleep so that desaturating patients had more time for desaturation to occur. Thus hypoventilation appears to be a primary factor in sleep O2 desaturation in these patients. Because of the fall in lung volume, maldistribution of ventilation may also contribute.