MECHANISM OF HALOTHANE-INDUCED TACHYPNEA IN CATS

The mechanism of the tachypnea induced in cats by increasing the halothane concentration from 1.2-3% was studied and the afferent vagal and the central component was quantified. Two variables were measured: the breathing frequency after occlusion of the airways at end-expiratory volume, and the rate of change of pressure developed in the airways during the inspiratory effort after occlusion of the airways. The former was taken as an index of the central timing of breathing, and the latter as an index of the respiratory output. Increasing halothane concentration under isocapnic conditions (PAC02 [arterial CO2 partial pressure] .apprxeq. 45 torr) caused an increase in frequency of occluded breaths from 25-35 cps (mainly achieved through a shortening of the inspiratory phase) and a decrease in the rate of change of occlusion pressure from -18 to -10 cm H2O/s. At either halothan concentration vagotomy or complete cold vagal block did not significantly modify the 2 respiratory variables considered. Apparently the excitatory effect of increasing halothane concentration on respiratory timing and the inhibitory effect on respiratory output were centrally and not vagally mediated.