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The liver receives about 25% of cardiac output. Portal blood accounts for about two-thirds of total flow, and although the liver does not regulate portal flow, it does regulate portal pressure. The hepatic arterial flow is regulated by a unique intrinsic regulatory system, the hepatic arterial buffer response, that is dependent on an adenosine washout mechanism and serves to hold total hepatic blood flow constant. Hepatic arterial flow is not regulated by liver metabolic demands, but rather subserves the hepatic role as a regulator of blood levels of nutrients and hormones by maintaining blood flow and thereby hepatic clearance, as steady as possible. The arterial buffer also plays a role in maintenance of intrahepatic pressures and liver volume. About 30% of hepatic volume is blood (12% of total body blood volume). This total capacitance consists of stressed and unstressed volumes. Stressed volume depends upon intrahepatic pressure and vascular compliance (distensibility). Unstressed volume is the theoretical volume remaining in an organ at zero pressure. Pressures and flows would not be altered if unstressed volume was absent. Active constriction of the capacitance vessels results in transfer of unstressed volume to stressed volume, which maintains or increases venous pressure and venous return. Passive volume changes, secondary to flow changes and thus intrahepatic pressure, are also dramatic in the liver and represent changes in stressed volume. Intrahepatic pressure is virtually equal to portal venous pressure in the normal basal state and is regulated by hepatic venous sphincters. Active hepatic vasoconstriction can result in contraction of these sphincters and also in some presinusoidal constriction. The sphincters appear to be passively distensible, and this characteristic serves to maintain portal and intrahepatic pressures at quite constant levels such that, if inflow decreases, the sphincter resistance increases, and pressure is prevented from a precipitous fall. The intrahepatic pressure maintains sinusoidal patency and allows all sinusoids to be uniformly perfused, even at quite low flows. Fluid and solute exchange between blood and the parenchymal cell is affected by the

SUMMARY1. In anaesthetized cats, the hepatic artery, portal vein and inferior vena cava pressures and the hepatic artery and portal vein flows were recorded using pressure transducers and electro-magnetic flowmeters.2. The hepatic nerves were stimulated with maximal stimuli for periods of 2-5 min. The magnitude of the response varied with the frequency of stimulation over the range 1-10 impulses/sec. The resistance to flow increased in both the hepatic artery and the portal vein.3. In the hepatic artery, mean pressure remained virtually constant, while the flow showed an initial marked decrease followed by a return towards the control level. In the portal vein, the flow remained constant while portal pressure showed a maintained increase. These responses were unaffected by previous administration of atropine and propranolol, but were blocked by phenoxybenzamine.4. Infusions of noradrenaline into the hepatic artery produced changes similar to those following stimulation of the nerves. In contrast, when the hepatic arterial pressure was maintained constant, intravenous infusions of noradrenaline produced a maintained decrease in hepatic artery flow.5. The occurrence of autoregulation of the hepatic artery flow at arterial pressures above 80-100 mm Hg was confirmed.6. Occlusion of the carotid arteries caused a rise in arterial pressure with little change in hepatic artery flow, but when the hepatic artery pressure was maintained at the pre-occlusion level the flow showed an abrupt decrease, usually followed by a recovery towards the control level. This decrease was abolished by section of the hepatic nerves and removal of the adrenal glands.

SU-MMAMY1. These experiments were designed to measure how much blood is mobilized from or pooled in the liver, spleen and gastro-intestinal tract to compensate for a haemorrhage or infusion of blood.2. Hepatic volume, splenic weight and intestinal volume were recorded in cats anaesthetized with sodium pentobarbitone. Whole blood was removed or infused at rates of 0-5-0-6 ml. kg-'. min-1 until 10 ml./kg (1 9 % blood volume) had been removed or 18 ml./kg (34 % blood volume) had been infused. These blood volume changes produced only small changes in arterial and portal pressures except after removal of 8 ml.fkg (1 5 % blood volume) when arterial pressure began to decrease rapidly.

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