Journal of applied physiology
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Regional ventilation and perfusion were studied in 10 anesthetized paralyzed supine patients by single-photon emission computerized tomography. Atelectasis was estimated from two transaxial computerized tomography scans. The ventilation-perfusion (V/Q) distribution was also evaluated by multiple inert gas elimination. ⋯ Little perfusion was seen in the most ventral parts (zone 1) of caudal (diaphragmatic) lung regions. In summary, shunt during anesthesia is due to atelectasis in dependent lung regions. The V/Q distributions differ from those shown earlier in awake subjects.
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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.