The introduction of transjugular intrahepatic portal-systemic stent-shunt (TIPSS) has been a major breakthrough in the treatment of portal hypertension, which has evolved to a large extent, into a routine procedure. A 21-year-old male patient with progressive graft fibrosis/cirrhosis requiring TIPSS for variceal hemorrhage in the esophagus due to portal hypertension was unresponsive to conventional measures two years after living related liver transplantation (LDLT). Subsequently, variceal hemorrhage was controlled, however, liver function decreased dramatically with consecutive multi organ failure. CT scan revealed substantial necrosis in the liver. The patient underwent successful "high urgent" cadaveric liver transplantation and was discharged on postoperative d 20 in a stable condition.

Dihydroergotamine (DHE) 0.02 mg X kg-1 was administered i.v. in 9 dogs with high epidural block. Mean arterial blood pressure was restored from 11.0 +/- 2.4 kPa to 18.8 +/- 2.5 kPa by DHE due to a near twofold increase in systemic vascular resistance while cardiac output was unchanged. Hepatic arterial blood flow was reduced by 50% by a marked increase in hepatic arterial resistance above the pre-epidural value, while portal venous blood flow remained unchanged. Hepatic oxygen consumption decreased following DHE in spite of an increase in total oxygen consumption, probably partly due to a reduction in hepatic arterial oxygen availability. The mechanism by which the arterial blood pressure is restored by DHE in dogs during high epidural block must be regarded as unfavourable, especially with respect to the liver.

The effects of increasing concentrations of nitrous oxide 30, 50 and 70% on the hepatic circulation and hepatic oxygen consumption were investigated in seven normocapnic greyhounds. Hepatic arterial and portal venous blood flows were measured continuously using electromagnetic flow probes, and mean arterial pressure and cardiac output monitored. The administration of nitrous oxide caused linear decreases in hepatic arterial, portal venous and total liver blood flows. Increases in mean arterial pressure, hepatic arterial resistance and mesenteric vascular resistance were noted. There were no significant changes in hepatic oxygen consumption. It is suggested that the decrease in liver blood flow may result from alpha-adrenoceptor stimulation.

The hepato-renal syndrome is defined as potentially reversible functional renal failure associated with acute fulminant hepatitis or, more often, with advanced chronic liver failure. It is characterized by oliguria, azotemia, retention of sodium and water with formation of ascites, and hyponatremia. While urinary sodium concentration of less than 10 mEq/l reflects intact tubular sodium absorption, the kidney lacks the ability for adequate free-water generation. This condition must be separated from specific renal diseases which may arise during the course of intra-or extrahepatic diseases and which must be classified accordingly. Pathophysiological aspects of the hepa-to-renal syndrome include hemodynamic factors, such as changes in intrarenal blood flow distribution in the presence of elevated intrarenal and reduced peripheral vascular resistance. The functional relationship of vasoconstrictor, sodium retaining, and anti-diuretic hormones (e.g., renin-angiotensin, aldosterone, and vasopressin) to vasodilator, diuretic, and natriuretic hormonal factors (e.g., prostaglandins, kinins, and natriuretic hormone) may be altered as well. Finally, a pre- and intrahepatic spillover resulting in decreased endotoxin clearance must be considered. Due to the lack of understanding of their complex interactions, so far pharmacological and therapeutic approaches remained ineffective to correct at least some of these factors. Today, recovery from hepato-renal syndrome will, therefore, mainly depend on the course of the underlying liver disease.

The acute effect of portal vein occlusion on hepatic arterial blood flow was studied in a group of nine anaesthetised dogs. The influence of hepatic artery denervation and total liver denervation on the hepatic arterial flow response was determined subsequently. Blood flows in the hepatic artery and portal vein were measured with electromagnetic flowmeters, and hepatic tissue perfusion with 85Krypton clearance. A side-to-side mesocaval shunt was constructed to provide a drainage channel for the mesenteric venous blood during the periods of portal vein occlusion. Occlusion of the portal vein produced an immediate and significant increase in hepatic arterial flow which was sustained at approximately 80% above control for the 6 min period of observation. Total liver blood flow and hepatic tissue perfusion were both significantly reduced by about 40%. Denervation either of the hepatic artery alone or the entire liver produced no change in the response, and it is concluded that there is no neurogenic component either initiating or modifying the early changes in hepatic arterial flow.

Inferior v. cava pressure (IVCP) was raised in the dog by a baloon catheter introduced via the jugular vein. Hepatic artery flow (HAF) and portal venous flow (PVF) were measured with the electromagnetic flow meter. The increase of IVCP reduced uniformly HAF and PVF, the relative contribution of the two vessels to the HBF did not change. The relationship between IVCP increase and HAF reduction and between the decrease of AP-IVCP and the reduction of HAF was linear. There was no sign of autoregulation or vasomotor regulation of HAF. The changes in IVCP are only partially transmitted to the portal venous pressure (PVP). There was no change in intrahepatic portal resistance with increased IVCP. The increase in PVP did not lead to resistance changes in the splanchnic circulation. As a sign of the autoregulation of splanchnic circulation of the AP-PVP versus PVF curve was concave to the pressure axis. It is concluded that as a result of opposing autoregulatory and vasomotor influences in the intact animal the hepatic circulation appears to react passively to the increased outflow pressure.

Ten dogs were subjected to a period of hypovolaemia (bleeding volume: 2% of body weight) and to a period of halothane anaesthesia (end-tidal halothane concentration: 1%). Mean arterial blood pressure decreased to 79% of control value during hypovolaemia and to 58% of control value during halothane anaesthesia. Mean total peripheral and preportal vascular resistances increased during hypovolaemia and were unchanged during halothane. Mean hepatic arterial and portal venous blood flows decreased to 82% and 55% of control values, respectively, during hypovolaemia, and to 41% and 56% of control value, respectively, during exposure to halothane. Mean hepatic arterial resistance was unchanged during hypovolaemia, but increased during halothane. Mean hepatic oxygen consumption did not change significantly during hypovolaemia, but decreased during halothane anaesthesia, in spite of an increased extraction of oxygen from both the hepatic arterial and the portal venous blood. Possible mechanisms which may maintain oxygen supply to the liver by increasing the hepatic arterial fraction of total liver blood flow when portal venous blood flow is reduced are discussed. It is concluded that this mechanism is upset or inhibited during halothane anaesthesia.

Continuous i.v. infusions of histamine (5 mug/kg - min), vasopressin (10 mU/kg -min), or angiotensin II (0.5 mug/kg - min) were given to fasting cats. Hepatic arterial flow was decreased 30% by histamine, increased 30% by vasopressin, and not significantly affected by angiotensin, whereas portal venous flow was increased 25% by histamine, decreased 40% by vasopressin, and not significantly affected by angiotensin. The hepatic arterial conductance was decreased about 25% by histamine and angiotensin, and not significantly affected by vasopressin. The gastrointestinal conductance was decreased about 40% by vasopressin and angiotensin, and increased 25% by histamine. The conductance in the intrahepatic low pressure vessels was not affected by histamine and vasopressin, but decreased 25% during the infusion of angiotensin. These hemodynamic effects, however, were not accompanied by changes in the liver function or hepatic metabolism as judged from the splanchnic elimination of ethanol, the hepatic uptake and excretion of ICG, the hepatic oxygen consumption, and lactate and ketone production. This indicates that the functional capacity of the liver and thereby the number of sinusoids perfused is not markedly influenced by these drugs. Vasopressin caused a decrease in the oxygen consumption and an increase in the lactate production in the prehepatic splanchnic area, which may be due to a redistribution of the gastrointestinal blood flow.

The oxygen supply to the liver was found to be dependent on the total blood flow only and not on the ratio of arterial to portal contribution. The mean value of O2-uptake in the liver, related to a blood flow of 110 ml/min - 100 g liver, amounted to 6.08 +/- 0.2 ml O2/min - 100 g liver (mean +/- S.E.M.). O2-uptake of the intestine was found to be 1.95 +/- 0.13 ml O2/min - 100 g tissue, related to a normal blood flow of 50 ml/min - 100 g tissue. With low oxygen supply O2 extraction in the liver reaches values of 97%, whereas the intestinal extraction does not surpass 75%. A rise in oxygen supply surmounting normal values does not increase the O2-consumption. Contrary to the intestinal circulation the liver showed no postocclusive vasodilatation. The oxygen debt was payed back by a greater extraction. The portal oxygen supply to the liver can markedly increase due to intestinal metabolic hyperemia. High O2-extraction capacity, rather than vasodilatation, is the main mechanism for matching hepatic oxygen supply with requirements. The hepatic venous blood may leave the liver with an extremely low O2-content.