The cholinergic component of CO2-induced cerebral vasodilatation in the rabbit will be analyzed pharmacologically and anatomically; the possible role of such a system in cerebral vascular responsiveness to O2 will be assayed. The reflex vagal bradycardia in response to hypoxia will be analyzed with respect to neural unit activity in the mesencephalon, and the possible interaction of this reflex with pulmonary and atrial reflexes. Assessment of the effects of type and epth of anesthesia on the distribution of blood flow during hypoxia and hypercapnia will be continued.