EFFECTS OF MEMORY FROM VAGAL FEEDBACK ON SHORT-TERM POTENTIATION OF VENTILATION IN CONSCIOUS DOGS

1. We assessed short-term potentiation of ventilation in response to brief systemic normocapnic hypoxaemia in conscious dogs. Four recumbent dogs were exposed to P(a, O2) 35-55 mmHg with P(a, CO2) maintained normocapnic for forty to fifty seconds and then abruptly returned to normoxia. Minute ventilation (V(I)) increased 4- to 5-fold during hypoxia due to both increased tidal volume (V(T)) and frequency (f). Several trials of hypoxic exposure with normoxic restoration were conducted with animals intact and following bilateral cold blockade of the cervical vagus nerves sufficient to block completely the Hering-Breuer reflex. 2. In the vagally intact dog, when normoxia was restored immediately following normocapnic hypoxia (P(ET, O2) = 40 Torr), expiratory time (T(E)) was prolonged to 190 +/- 68 % of control (mean +/- S.E.m., range 53-350 %) on the second or third breath and then returned slowly to control values on subsequent breaths. The prolongation of T(E) following removal of the hypoxic stimulus was positively correlated with the magnitude of the peak V(T) reached during hypoxic exposure. However, V(T) and V(I) remained significantly greater than control over a twenty second or four-breath period following hypoxia. 3. In the vagally blocked dog, no prolongation of T(E) was observed following isocapnic hypoxia; nor was T(E) following hypoxia correlated with the magnitude of the V(T) during hypoxia. The time constants of decay of V(I), V(T) and f back to control, following hypoxia averaged 16, 19 and 9 s, respectively. 4. We conclude that short-term potentiation of ventilatory output following peripheral chemoreceptor hypoxic stimulation does exist in the awake dog, but the stimulatory after-effect is masked and T(E) is prolonged by a 'memory' of inhibitory vagal feedback. The magnitude of this inhibitory after-effect on T(E) prolongation increases in proportion to the increase in tidal volume achieved during the hypoxaemia. 5. This inhibitory effect of vagal memory may contribute to instability of breathing pattern and apnoea following transient disturbances in ventilatory output.