Journal of applied physiology
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The purpose of this study is to investigate the effect of chest wall configuration at end expiration on tidal volume (VT) response during CO2 rebreathing. In a group of 11 healthy male subjects, the changes in end-expiratory and end-inspiratory volume of the rib cage (delta Vrc,E and delta Vrc,I, respectively) and abdomen (delta Vab,E and delta Vab,I, respectively) measured by linearized magnetometers were expressed as a function of end-tidal PCO2 (PETCO2. The changes in end-expiratory and end-inspiratory volumes of the chest wall (delta Vcw,E and delta Vcw,I, respectively) were calculated as the sum of the respective rib cage and abdominal volumes. ⋯ The group delta Vab,I/delta PETCO2 slope (0.004 +/- 0.014 1/Torr) was not significantly different from zero despite the VT nearly being tripled at the end of CO2 rebreathing. In conclusion, the individual VT response to CO2, although independent of delta Vab,E, is a function of delta Vrc,E to the extent that as the delta Vrc,E/delta PETCO2 slope increases (more positive) among subjects, the VT response to CO2 decreases. These results may be explained on the basis of the respiratory muscle actions and interactions on the rib cage.
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The purpose of this study was to determine the effect of inhibition of nitric oxide (NO) release on the diaphragmatic microvascular responses to hypoxia. In alpha-chloralose-anesthetized mongrel dogs, the microcirculation of the vascularly isolated ex vivo left hemidiaphragm was studied by intravital microscopy. The diaphragm was pump perfused with blood diverted from the femoral artery through a series of membrane oxygenators. ⋯ L-NNA eliminated the increase in blood flow during moderate hypoxia and inhibited arteriolar dilation by an amount that was related to vessel size (i.e., dilation of larger vessels was inhibited more than that of smaller vessels). Inhibition of NO synthesis had no effect on the increase in diaphragmatic blood flow (23.6 +/- 1.9 ml.min-1.100 g-1; P > 0.05 compared with that during severe hypoxia before treatment with L-NNA) or arteriolar diameters during severe hypoxia. NO release plays a role in the diaphragmatic vascular response to hypoxia, but this role is limited to dilation of larger arterioles during hypoxia of moderate severity.
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A sinusoidal forcing function inert-gas-exchange model (C. E. W. ⋯ When arterial blood is not fully saturated, the theory predicts that QS/QT is directly related to the ratio of the amplitudes of the induced-saturation sinusoids in arterial and mixed-venous blood. The model therefore predicts that 1) on-line calculation of airway dead space and end-expired lung volume can be made by the addition of an oxygen sine-wave perturbation component to the mean FIO2; and (2) QS/QT can be measured from the resultant oxygen perturbation sine-wave amplitudes in the expired gas and in arterial and mixed-venous blood and is independent of the mean blood oxygen partial pressure and oxyhemoglobin saturation values. These calculations can be updated at the sine-wave forcing period, typically 2-4 min.
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Clinical Trial
Breathing and brain blood flow during sleep in patients with chronic mountain sickness.
Chronic mountain sickness (CMS) patients have lower arterial O2 saturation (SaO2) during sleep compared with healthy high-altitude residents, but whether nocturnal arterial O2 content (CaO2) and brain O2 delivery are reduced is unknown. We measured SaO2, CaO2, sleep-disordered breathing (SDB), and internal carotid artery flow velocity in 8 CMS patients, 8 age-matched healthy CMS controls, 11 healthy younger-aged Han, and 11 healthy younger-aged Tibetan male residents of Lhasa, Tibet (3,658 m). CMS patients spent a greater portion of the night in SDB (total no. of episodes of apnea, hypopnea, and hypoventilation) than did the CMS controls, young Han, or young Tibetans (15% vs. 5, 1, and 1%, respectively; P < 0.05) because of more frequent apnea and hypoventilation episodes and longer duration of all types of episodes. ⋯ Whereas flow velocity remained elevated from awake to rapid-eye-movement sleep in the CMS controls, it fell in the CMS patients. During episodes of SDB, internal carotid flow velocity increased in CMS controls but did not change in the CMS patients such that values were lower in the CMS patients than in CMS controls at the end and after SDB episodes. We concluded that SDB and episodes of unexplained desaturation lowered nocturnal SaO2 and CaO2, which, together with a lack of compensatory increase in internal carotid artery flow velocity, likely decreased brain O2 delivery in CMS patients during a considerable portion of the night.
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A companion paper (C. E. W. ⋯ Under hyperoxic conditions, intravascular oxygen sensors confirmed that the sinusoidal PO2 signal passed into the arterial blood but not into the mixed-venous blood. However, the sinusoid perturbation PO2 signal did pass into the mixed-venous blood when the mean FIO2 was mildly hypoxic (FIO2 = 0.18% vol/vol). These data show that oxygen can be used instead of argon to measure airways dead space and VA.