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At least 19 recordsLinked to original sources

Liver circulation and oxygen metabolism during short time ligation and the hepatic artery in the dog.

The changes of liver circulation and liver oxygen metabolism during and after one hour hepatic artery ligation (HAL) were studied in eight mongrel dogs. At the end of the HAL period total hepatic blood flow (THBF) was reduced from 115.6 +/- 5.5 ml/min . 100 g liver tissue to 68.0 +/- 3.7 ml/min . 100 g or 59% of the initial value. The portal venous blood flow was reduced from 83.1 +/- 3.4 to 58.8 +/- 3.7 ml/min . 100 or 82% of the initial value and the liver oxygen consumption was reduced from 4.1 +/- 0.2 ml/min . 100 g to 3.1 +/- 0.3 ml/min . 100 g or 76% of the initial value. The changes in portal venous blood flow and liver oxygen consumption were reversible following reopening of the hepatic artery. The clinical importance of a reduced portal venous blood flow and liver oxygen consumption following HAL and the possibilities to increase the portal venous blood flow are discussed.

Animals

[New aspects of liver circulation: effects and consequences for the portocaval shunt therapy in liver cirrhosis].

Hepatic circulation, which is of essential importance in supplying the liver cells with oxygen and substrates needed for securing metabolic homeostasis of the organism, is characterized by well-regulated mechanisms of intrahepatic arterial, portal and hepatovenous interaction. Furthermore, the hepatic circulation is integrated in the systemic and splanchnic hemodynamic as interposed in a high, or respectively low, pressure system. Beside these hemodynamic mechanisms there are also specific morphologic features in the hepatic vascular bed responsible for regulating liver blood flow. For hepatic nutritions and trophics, and for the metabolic homeostasis of the organism, portal blood is of greater importance than arterial. In porto-caval shunt surgery it is recommended that any remaining portal flow to the liver be preserved to the greatest extent possible.

Homeostasis

[Liver circulation under the effect in intestinal hormones in patients with diabetes mellitus].

The following significant disturbances of the blood flow were revealed in the liver of 104 patients suffering from diabetes mellitus as a result of rheographic studies: a reduction of the amplitude-frequency index, of the sphygmometric velocity and of its components--the rate of rapid and slow blood filling. The intestinal hormones--secretion and cholecystokinin-pancreosimin improved these indices. The duration of their effect (1.5 U/kg, intravenously) was not less than 20, and not less than 10 min, respectively.

Adult

[Hemodynamic studies on liver circulation with special reference to the hepatic artery].

Hepatic and systemic hemodynamics were studied in the rat under different experimental conditions. It could be demonstrated that the hepatic arterial blood flow in normal as well as in sick liver of animals is well regulated: for example by means of the venovasomotorical reaction (portoarterial interaction) and systemically by autoregulation. There exists an inverse correlation between arterial and portalvenous liver blood flow: As portal liver blood flow decreases hepatic arterial flow increases. Especially a marked increase of hepatic artery flow was found after portocaval end-to-side anastomosis. Yet, the hepatic artery flow improvement after portocaval shunt could not compensate the diverted portalvenous blood supply at all. In states of portal hypertension with a relevant portocaval collateral circulation, also after surgical portocaval shunt, the systemic circulation becomes more hyperdynamic. There also exists a remarkable relation between the extent of portocaval shunt flow to circulating blood volume, cardiac output and circulation time. Some correlates of the experimental findings with the altered hemodynamics in human liver cirrhosis were found and discussed from the viewpoint of portocaval shunt surgery in man.

Animals

[Measurement of liver circulation by means of an ultrasonic Doppler flow measuring device].

The ultrasonic-Doppler technique is a very simple method for flow measurement. With this method the generally accepted mechanism of hepatic arterial flow increase after reduction or interruption of the portal vein flow could be confirmed. The increase was not related to cardiac output. Previous doubts about the portal vein flow behaviour after suppression of hepatic artery flow were decided, joining the little group of authors, who did not observe a variation of the portal vein flow in this condition. The concept of the autoregulation of the liver blood supply seems to be connected to the hepatic arterial system only. Although an increase of the hepatic artery flow after infusion of isoproterenol supports the existance of beta-receptors in the hepatic arterial system, it could be proved, that there was no reduction after propranolol infusion. This suggests, that autoregulation of the liver blood supply is not connected to the beta-receptors only.

Animals

[Liver circulation during dopamine therapy].

Intravenous dopamine (4 and 8 microgram/kg/min) causes an increase of hepatic flow and cardiac index, while the ratio hepatic flow:cardiac index remains unchanged. The increase of renal flow after dopamine therefore does not occur at the expense of hepatic flow.

Cardiac Output

Direct effects of various catecholamines on liver circulation in dogs.

As measured by electromagnetic blood flow transducers, direct infusion of epinephrine, norepinephrine, and dopamine into the portal vein (PV) produced a 40-50% decrease in hepatic arterial (HA) blood flow; isoproterenol increased HA flow by about 69%. No changes in PV flow or pressure were observed. Direct HA infusion of the vasoconstrictors decreased HA flow by amounts comparable to those occurring after PV infusion. However, HA infusion of isoproterenol increased HA flow only 15% suggesting a difference in beta-receptor population in the two vessels. When infused directly into the superior mesenteric artery (SMA), epinephrine and norepinephrine reduced SMA flow by about 45% and PV flow by 20-25%; HA flow increased 6-8%. Infusion of isoproterenol and dopamine into SMA increased SMA flow by 115% and 206% and PV flow by 60% and 70%, respectively, whereas HA flow decreased by 25% and 50%. Portal vein pressure increased less than 3 mmHg. Alpha- and beta-receptor blockade of the liver did not change significantly the alterations in hepatic arterial blood flow that were secondary to changes in portal venous blood flow. It is likely that regulation of hepatic arterial flow resides in mechanisms located within the liver sinusoids.

Adrenergic beta-Antagonists

[Umbilical collateral circulation in liver cirrhosis - Cruveilhier-v. Baumgarten syndrome (author's transl)].

Embryonal development and anatomy of the liver are shortly discussed; they do explain collateral circulation in liver cirrhosis. A case report is given of a patient with umbilical collateral circulation (Cruveilhier-v. Baumgarten syndrome), exhibiting impressive clinical and radiological findings. Such an umbilical collateral circulation will develop in up to 21% of all patients with an intrahepatic block. This is only one variant - not prone to complications by the way - of a multitude of different portosystemic shunts in liver cirrhosis. Therefore it should not be talked about as an independent syndrome.

Collateral Circulation

The circulation in liver tissue and experimental liver metastases before and after embolization of the liver artery.

Simultaneous measurement of cardiac output distribution with 86Rubidium and 57Cobalt-tagged microspheres in rats implanted with liver tumors by intraportal injection of sarcoma cells enables quantitation of arterial and portal tumor circulation. The portal circulation was found to be increased in small tumors as compared to the liver, but as the tumor grew there was a decrease in the portal tumor circulation. When the tumor growth became massive even the total liver circulation was reduced, as measured with 133Xenon wash-out. All the tumors had increased arterial circulation. This arterial hyperperfusion was changed into ischemia when the liver artery was occluded through embolization with degradable microspheres.

Animals