Cardiovascular changes associated with augmented breaths in normoxia and hypoxia in the rat.

1. In the present study, anaesthetized rats showed respiratory gasps (augmented breaths) at regular intervals during air breathing and at increased frequency during hypoxia (breathing 15, 12, 8 or 6% O2 in N2). Each augmented breath was accompanied by transient vasodilatation in hindlimb skeletal muscle and sometimes bradycardia. In hypoxia these changes were superimposed upon more gradual muscle vasodilatation and tachycardia. 2. Both the augmented breaths and the transient muscle vasodilatations disappeared immediately after bilateral vagotomy but both sometimes reappeared 1‐2 h later, particularly in hypoxia. 3. The transient vasodilatation in skeletal muscle sometimes preceded the augmented breath, indicating that the vasodilatation was not a reflex initiated by pulmonary stretch receptors secondary to the augmented breath. Moreover, hyperinflation of the lungs to 5‐10 mmHg evoked the Breuer‐Hering respiratory reflex but had no effect upon the cardiovascular variables. 4. Addition of SO2 (300‐400 p.pm.) to the inspirate, which others have shown preferentially blocks pulmonary stretch receptors, abolished the Breuer‐Hering reflex, but had no significant effect on baseline levels of muscle vascular conductance or heart rate during normoxia, nor on the gradual increases in these variables during hypoxia (8% O2). Moreover, augmented breaths still occurred during air breathing and during hypoxia, each being associated with transient muscle vasodilatation. 5. These results indicate that pulmonary stretch receptors have little reflex effect upon the cardiovascular system of the rat either in normoxia or hypoxia. Rather, we suggest that transient muscle vasodilatation and possibly bradycardia, as well as an augmented breath, are all part of a primary reflex, initiated by pulmonary irritant receptors, and facilitated by peripheral chemoreceptor stimulation, repetition of which is an integral part of the response to hypoxia.