Summary Inhalation and perfusion lung scans were performed in 15 patients with bronchial asthma, during an exacerbation and during a relatively symptom‐free phase in each patient. The inhalation scans were obtained using an aerosol containing a Tc99m‐iron complex, the perfusion scans with intravenously injected I131 macro‐aggregated albumin. The pulmonary distribution of both inhaled and injected material was uneven in all 15 patients during exacerbations of asthma. The distribution of both inhaled and injected material became more even as the patients recovered. The limitations of an inhaled radio‐active aerosol as an indicator of uneven distribution of ventilation were explored. In particular, it was found that aerosol was selectively deposited on sputum lying proximally in the bronchial tree. In five patients during an exacerbation of asthma, the distribution of isotope in the perfusion scan was very similar to the distribution of isotope in the inhalation scan. This indicates fairly good matching of blood flow distribution with abnormal ventilation distribution on a topographical basis in such patients.
Summary. The in vivo titration curve of CO, measured in five subjects during rebreathing of 7% COg in O2 for 3 minutes was not significantly different from the corresponding in vitro titration curve measured on arterial blood from each subject. The buffering of COg m vivo when measured by other methods is known to be less than it is in vitro. COj in vivo is thought to equilibrate with a well buffered compartment (intravascular) and a poorly buffered compartment (interstitial fiuid). It has been suggested that HCO3-shift takes place from the intravascular compartment. During rebreathing there may be insufficient time for HCO3-shift to occur. This would explain the identical COg titration curves in vivo and in vitro shown by this study. INTRODUGTION.The GO2 titration curve of whole blood in vivo has been obtained by exposing normal man and dogs to progressively higher levels of inspired GOî n the presence of normoxia, hyperoxia and hypoxia (Gohen, Brackett and Sehwartz, 1964; Brackett, Gohen and Schwartz, 1965; Brown and Glancy, 1965;Michel, Lloyd and Gunningham, 1966; Mithoefer, Karetzky and Porter, 1968). With these methods GO2 titration curves are constructed from measurements on blood samples after equilibration of GO2, H+ and HGOs" in intracellular, interstitial and intravascular compartments has taken place. The resulting GO2 titration curves are different from the in vitro GOo titration curves of whole blood. The HGOa" concentration is less than predicted from the in vitro GO2 curve. It is thought that loss of HGO,,-from blood to interstitial fluid takes place (Shaw and Messer, 1932;Michel et al, 1966). This paper reports the GO2 titration curve in man of whole blood in vivo obtained during rebreathing of 7% GO2 in O2 (Read, 1967). During rebreathing a rapid and progressive increase of arterial H+ and arterial PCO2 occurs. The rate of increase of arterial PCO2 is about 6 mm. Hg./min. A comparison of this in vivo curve with the corresponding in vitro GO2 titration curve enables certain inferences about the rate of HGO3"" exchange to be made. MATERIALS AND METHODS.Five male patients with obstructive lung disease (age range 15-63 years) were studied. All had been referred for assessment of respiratory function and this provided the opportunity
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