Pulmonary resistance during halothane anesthesia is not determined only by airway caliber

Studies of the effect of halothane on airway smooth muscle have used pulmonary resistance as an index of airway caliber. However, pulmonary resistance (R(L)) is the sum of airway resistance (R(aw)), which changes with airway caliber, and of tissue resistance (R(ti)), which depends on the pressure-volume hysteresis of the lung. To separate the effects of halothane on airway caliber from its possible effects on tissue pressure-volume hysteresis in the unstimulated lung and during bronchoconstriction, the authors measured both components of R(L) before and during vagus nerve stimulation in 12 dogs before and during halothane administration R(ti) was always the major component of R(L), constituting 77 ± 14% (mean ± SD) or R(L) before vagus nerve stimulation and 64 ± 21% of R(L) during stimulation in the absence of halothane. Vagus nerve stimulation caused approximately equal increases in both R(ti) and R(aw). Halothane attenuated the response of both R(ti) and R(aw) to vagus nerve stimulation in a dose-dependent fashion. At 1 MAC, the R(ti) response was 44 ± 13% of its value before halothane administration and the R(aw) response was 32 ± 12% of its value before halothane administration; these responses were not significantly different. The authors conclude that changes in R(L) during halothane administration are caused not only by changes in airway caliber, as previously assumed, but also reflect a significant effect of halothane on lung tissue pressure-volume hysteresis.