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1. Cerebral blood flow, oxygen and glucose consumption, hind-limb blood flow and oxygen consumption, blood pressure and heart rate were measured in seven ventilated dogs. 2. Inhalation of 5% CO2 caused a significant increase in cerebral blood flow and a significant decrease in cerebral glucose utilization. 3. Isoprenaline infusion (0·4 μg kg−1 min−1) caused a rise in cerebral blood flow, oxygen and glucose consumption. There was also an increase in peripheral blood flow and in most instances an increase in peripheral oxygen utilization. 4. The inhalation of 5% CO2 during isoprenaline infusion abolished the increase in cerebral blood flow, in cerebral glucose consumption and heart rate. Cerebral oxygen consumption was significantly decreased to below control values. Once the administration of 5% CO2 was discontinued an increase in peripheral oxygen consumption became apparent. 5. The possible therapeutic implications of these findings are outlined.

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SYNOPSIS Ammonium acetate (13 m-mol), ammonium bicarbonate (13 m-mol), and ammonium hydroxide (30 m-mol) were administered intravenously to three separate groups of five dogs. Ammonium acetate and bicarbonate were given over a period of 15 minutes, ammonium hydroxide was given for 30 minutes. In all dogs, after 15 minutes' infusion, the blood ammonia concentration was similar to that found in patients with hepatic coma. When the ammonium hydroxide had been given for 30 minutes, lightening of anaesthesia was noted in all dogs studied. At this time blood ammonia values were over 1,000 ,g/100 ml in two animals. Subsequent deepening of anaesthesia was observed after termination of the infusion. In all animals studied there was an increase in cerebral glucose consumption with little change in oxygen utilization. Arterial lactic acid was studied in the group given ammonium bicarbonate and found to increase at the same time as the increase in glucose utilization. Hyperventilation was precipitated by both acid and alkaline ammonium salts. Lactic acidosis appeared to be the cause rather than the result of the hyperventilation. The protective effect of hyperventilation on brain metabolism is discussed.The role of ammonia in the genesis of hepatic coma is still far from clear. Thus, while in hepatic coma there is an elevation of blood ammonia and a reduction in cerebral oxygen utilization, the correlation between these two variables is poor (Fazekas et al., 1956). The infusion of ammonium acetate into dogs was shown some years ago (James et al., 1971) to cause a reduction in cerebral oxygen consumption. However, these experiments were performed in dogs whose ventilatory rate and depth were kept constant throughout and thus compensatory hyperventilation was impossible. Since hyperventilation is common in patients with chronic liver disease (Vanamee et al., 1956) and since the respiratory alkalosis is thought in these circumstances to be compensatory, acting to protect rather than to impair brain function (Posner and Plum, 1966), it seemed important to evaluate the effect of ammonium salts in freely ventilating animals as well as in those in whom the ventilation had been controlled. METHODSThe experiments were carried out on 15 mongrel

1. Changes in brain and hind-limb blood flow and metabolism have been studied in six dogs before and after the acute shunting of portal vein blood into the systemic circulation.2. An initial increase in brain blood flow, oxygen and glucose consumption was found.3. More prolonged shunting caused a fall in flow and in oxygen and glucose utilization by the brain. Although peripheral blood flow and oxygen consumption were reduced byshunting glucose consumption was increased throughout the period of shunting.5. The possible mechanisms of these changes is discussed, together with their relevance to the causation of encephalopathy in patients after portacaval shunts.