This study elucidates the complex afferent interactions and central mechanisms mediating heart rate control during hypoxia and hyperventilation in rabbits.
Baroreceptor mean arterial blood pressure-heart period curves were obtained for unanesthetized sham-operated, thalamic, or pontine rabbits at an arterial Po 2 of 100 or 30 mm Hg. Each curve was S-shaped: it had a lower heart period plateau below threshold pressure, a part where heart period increased monotonically with rising mean arterial blood pressure, and an upper heart period plateau above upper saturation pressure. In spontaneously breathing rabbits, the pressure-dependent parameters of the curves were altered during hypoxia; in addition, there were baroreflex-independent shifts in heart period plateau levels. Suprapontine centers participated in both of these changes. An afferent analysis performed in rabbits treated with atropine and subjected to controlled ventilation showed that the changes in curve parameters were due to afferent interactions in cardiac sympathetic motoneurons between (1) arterial baroreceptor and chemoreceptor inputs which increased threshold, (2) arterial baroreceptor and cardiopulmonary baroreceptor inputs which lowered threshold and increased gain, and (3) cardiopulmonary baroreceptor and chemoreceptor inputs which increased gain and heart period range. Baroreflex-independent shifts in plateau levels were due to increased chemoreceptor and lung inflation receptor activity. The baroreflex-dependent and the baroreflex-independent components of the heart period response were mediated (as in spontaneously breathing rabbits) through both suprapontine centers and pontine centers.
Körner et al. (1973) studied this question.