Cerebral blood flow was measured using 133 xenon in forty-five baboons lightly anesthetized with pentobarbital. Blood flow varied between 62 and 82 ml/lOOg/min in gray matter and between 15 and 21 ml/lOOg/min in white matter. Hypercapnia and hypoxia caused a rise in blood flow and a fall in vascular resistance. Blood flow was independent of mean arterial blood pressure over the range 60 to 130 mm Hg. Section of the cervical sympathetic nerve enhanced the vascular response to CO 2 . Stimulation of the sympathetic nerve caused a reduction in blood flow in proportion to the initial blood flow. Similarly, after sympathectomy, blood flow was uniformly higher than control over the range of Pa 0o tested (35 to 450 mm Hg). After sympathectomy, blood flow was little different from control at low blood pressure but was higher within the physiological range and blood flow then fell steadily as pressure was reduced. When the carotid, vagus, and aortic nerves were cut in the neck, the blood flow response to hypoxia and hypercapnia was reduced, and when the aortic or vagus nerves were stimulated centrally, blood flow increased independently of Pa c0 ,,-Section of the seventh cranial nerve caused small and variable changes in blood flow, but if the vagus nerves had previously been sectioned, stimulation of the seventh cranial nerve caused an increase in blood flow in some of the tests. These results indicate that cerebral blood vessels are under reflex control. Possible receptors and pathways involved are discussed.

Preganglionic cervical and splanchnic sympathetic activity was recorded before and during administration of inhalation anaesthetics, in rabbits ventilated with oxygen and given gallamine. During control periods, when light anaesthesia was maintained with pentobarbitone, sympathetic discharge responded to changes in arterial pressure. Increased arterial Pco 3 exaggerated the amplitude of the respiratory sympathetic rhythm, and had a more variable effect on the mean impulse discharge rate. Preganglionic activity was increased by 25-50 per cent cyclopropane, which usually raised arterial pressure; by halothane, which caused severe hypotension; and by diethyl ether, which produced smaller circulatory changes. These experiments question the concept of "central vasomotor depression" during inhalation anaesthesia in the rabbit. Changes in preganglionic sympathetic activity produced by inhalation anaesthetics have not been studied directly apart from a brief communication by Martin and Marrazzi (1942), stating that cyclopropane and chloroform do not affect cervical sympathetic discharge in cats. Deutsch, Linde and Price (1962), however, measured an increased plasma adrenaline level during cyclopropane anaesthesia in the dog, while in the same species Millar and Morris (1960) found no increase in circulating catecholamines when halothane was given. The former result suggests that excitation of the sympathetic nervous system by cyclopropane may account for the arterial hypertension which usually occurs. This view is supported by head perfusion experiments (Price et al., 1963), also in the dog, while similar studies suggest that there is depression of central sympathetic discharge during halothane anaesthesia (Price, Linde and Morse, 1963), which accords with the reduced arterial pressure and the catecholamine measurements.

In rabbits which were ventilated mechanically, with a background anaesthetic of pentobarbitone or after decerebration, ketamine depressed preganglionic sympathetic activity and arterial pressure. Conduction through central baroreceptor pathways, tested by depressor nerve stimulation, showed a selective inhibition of the heart rate response.

The intravenous administration of the antiadrenaline drug phenoxybenzamine (Dibenzyline) markedly raised the arterial adrenaline and noradrenaline concentration in dogs lightly anaesthetized with thiopentone. Graded haemorrhage led to a further rise in the amounts of amine. In adrenalectomized dogs, phenoxybenzamine moderately increased the plasma noradrenaline concentration. During haemorrhagic hypotension, previous treatment of adrenalectomized animals with phenoxybenzamine led to a significantly greater rise in plasma noradrenaline compared with that of adrenalectomized animals subjected to haemorrhage without treatment with phenoxybenzamine. Thus, phenoxybenzamine (1) raised plasma amine concentration largely due to adrenal medullary stimulation, and (2) led to increased plasma noradrenaline concentrations during sympathetic stimulation in adrenalectomized animals. The previous administration of phenoxybenzamine reduced the amount of blood which could be withdrawn before final circulatory collapse in both normal and adrenalectomized dogs.