However, while studies of the acute effects of bronchodilation on arterial blood gases and V/Q relationships in asthma have been reported, there are, to our knowledge, no published reports specifically examining the effects of histamine-induced bronchoconstriction on V/Q relationships. In a study primarily concerned with the pulmonary vasodilator actions of nifedipine, Ballester et al found a smaller decrease in Pa02 (mean decrease 11.5 mm Hg) following methacholine-induced bronchoconstriction in mild asthma. The difference in magnitude can probably be accounted for by differences in the study population. Foppius and Stenius reported only a small decrease (mean —1.1 percent) in arterial 02 saturation (SaOa), measured with an ear oximeter, during histamine inhalation; changes in Sa02 and peak expiratory flow rate were only monitored for 90 s, before bronchoconstriction was reversed with isoproterenol inhalation. This may explain the difference in the magnitude of the induced hypoxemia between their report and the present study; in addition, small inaccuracies in Sa02 measurement in the range of P&02 in these subjects could mask relatively large changes in Pa02, and, finally, the degrees of induced bronchoconstriction between the two studies were probably not comparable. Other studies have examined the effects of bronchoconstriction on radioisotope-measured V/Q matching; these studies report that major changes occurred in ventilation distribution after histamine, with little change in the distribution of perfusion. read
In the present study, we utilized measurements of arterial blood gases and dead space to define V/Q abnormalities. While newer techniques of assessing V/Q relationships utilizing inert gases have been described, these are very complex and require steady state conditions, which would have been difficult to achieve during histamine inhalation. The concept of dead space ventilation, originally described over a century ago, remains valid for analyzing V/Q relationships. Since unclear definitions in the past have bedeviled discussions of respiratory dead space, in the present study we have adhered to currently accepted definitions; thus, the anatomic dead space (VDan), as measured from the expired C02 concentra-tion-volume trace, is synonymous with the series or airways dead space and extends from the lips to the interface between inspired and alveolar gas, in the respiratory bronchioles. The physiologic dead space, as measured in the present study, consists of the sum of VDan and the alveolar (VdA) or parallel dead space.