No abstract

No abstract

In an earlier paper (Andrews, Hecker, Maegraith & Ritchie, 1955) we described the actions of adrenaline, noradrenaline, acetylcholine and histamine on the perfused canine liver. In this paper we record briefly a study of the action of the same substances on the livers of the monkey, cat and rabbit. The work has been carried out in order to assess differences in the reactions of the hepatic vessels of these mammals. We were especially interested in the part played by the hepatic veins in the control of liver blood flow. METHODS ApparatusThe apparatus used was based on that described by Andrews (1953), but was modified to work with an extra-hepatic fluid volume of 150 ml. It is illustrated in the text diagram and is described below.From the hepatic veins the blood was conducted via an outflow recorder (Andrews, 1952) and a nylon filter to the main reservoir. From here it was pumped to a Hooker oxygenator, at whose base was a small chamber which acted as an upper constant-level reservoir. The excess of blood drained back via an outflow tube to the main reservoir. The upper reservoir was approximately 40 cm above the level of the liver, and blood flowed from it to the liver via a water-bath which was placed between the hindlegs of the animal. In the water-bath the blood stream was warmed to body heat and then passed to either the portal or arterial systems.The pressure within the portal vein was measured by a manometer, and was adjusted to physiological levels by means of a screw clamp. Variations of pressure were recorded by an inverted piston volume recorder, the kymographic tracings indicating changes in rate of flow. The majority of experiments were performed with a portal pressure of 7-10 cm blood. It was found necessary to include a bubble-trap in the circuit. Both glass and metal portal cannulae were used: for small animals metal was more suitable, and shortened, wide-bore, stainless-steel aspiration needles proved excellent.

No abstract

Summary Acetazolamide is shown to increase the urinary excretion of sodium and the sodium to potassium ratio in seven normal subjects and five cirrhotic patients without ascites. In seven cirrhotic patients with ascites the urinary output of sodium and the sodium to potassium ratio were low initially, and were unchanged by acetazolamide. The subjects with ascites had no evidence of renal disease, and the failure to excrete sodium must be attributed to an extrarenal factor. These observations are compatible with the hypothesis that there is an excessive secretion of aldosterone, though they do not indicate the cause. It is not necessarily lowering of plasma sodium level, as the abnormality of sodium and potassium excretion was also noted in one subject with a high normal plasma level. Liver disease also is not essential, as similar sodium retention occurred in one subject whose ascites was due to extrahepatic portal hypertension. Acetazolamide is found not to be a good diuretic in patients suffering from liver disease.