Abstrakt
To determine its role in the biphasic ventilatory response to hypoxia, we examined the diaphragmatic activity at its peak (DI), at the end of expiration (DE), and ventilation in adult anesthetized rats: (1) after 10 min of graded levels of poikilocapnic hypoxia (16, 14, 12, 10% O-2); (2) at 1, 5 and 10 min of steady hypoxia (10% O-2) in intact and vagotomized rats. (1) Gradual hypoxia progressively increased (V) over dot e and DE but DI only at 10% O-2; (2) 10% O-2 induced an initial increase in ventilaiton followed by its consistent decline. VT, DI and DE at first increased, then VT and DI decreased, while DE remained augmented.
VT and phasic activation of the diaphragm (DI - DE) decreased in parallel. Bilateral vagotomy did not affect the biphasic response of (V) over dot e.
These results suggest that (1) the increased end-expiratory activity of the diaphragm limits its phasic inspiratory activation and thus contributes to the biphasic character of the ventilatory response to sustained hypoxia; (2) vagal input does not play a major role in this phenomenon.