Journal of applied physiology
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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.
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Whether CO2 partial pressure (PCO2) in expired gas may exceed that in arterial blood has been controversial. We measured arterial PCO2 (Paco2) and end-tidal PCO2 (PETco2) in four awake goats during air breathing and during hyperoxic CO2 rebreathing in various conditions of acid-base balance. ⋯ Magnitude of the negative difference during rebreathing was too great to be accounted for by incorrect assumptions or measurement error, even if reasonable contributions from all known sources of error were concurrently invoked. We conclude that during hyperoxic CO2 rebreathing in goats, PETco2 exceeds Paco2.
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Rat lungs were perfused in an in vitro circuit with separate control of alveolar and pulmonary arterial O2 tension. With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes of perfusion pressure. ⋯ Where RA-v is this pressure response expressed as a percent of the maximum, the linearized form of the response surface is given by log [RA-v/(100-RA-v)] = 3.93 - 1.029 (log PvO2) - 1.623 (log PAO2). From this relationship it was concluded that 1) HPV is determined by PAO2 and PvO2; 2) the fundamental stimulus-response relationship is a sigmoid with a 50% response when both PAO2 and PvO2 are 30.3 Torr; 3) PAO2 has a greater effect than PvO2 due in part to the geometry of the vascular wall but principally due to O2 exchange between alveolar gas and blood in small pulmonary arteries; 4) there is not a localized sensor for HPV (the response is accounted for by each smooth muscle cell in the pulmonary arterial wall responding to the O2 tension in its vicinity); and 5) the characteristics of the response suggest that the cell sensor resembles a cytochrome.