Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIVER CIRCULATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1990

[The effect of catecholamines on blood circulation in the liver].

In acute experiments on dogs under nembutal anaesthesia the pressure and blood flow in the vessels supplying the liver have been recorded simultaneously with registration of the hepatic blood content changes. Catecholamines injected into liver vessels have been found to change significantly the liver circulation: adrenaline and noradrenaline evoke the constriction of intrahepatic vessels and decrease the blood content in the liver, realising through the alpha-adrenoreceptors activation, isadrin causes a weak vasodilatation by the activation of beta-adrenoreceptors. A selective inactivation of isadrin in the liver is shown. The density of alpha-adrenoreceptors distribution in the intrahepatic vessels is large enough and apparently some times exceeds the density of beta-adrenoreceptors. In 1/3 of dogs the beta-adrenoreceptors in the liver vascular bed are absent at all or present in arterial bed only.

Animals↗
PubMed1982

Physiological regulation of the hepatic circulation.

Liver blood flow is determined at normal arterial pressure by 1) the hepatic arterial vascular resistance, 2) the inflow resistance to the preportal vascular beds, 3) the intrahepatic portal venous vascular resistance. Hepatic arterial vascular resistance and therefore blood flow are regulated by relatively weak intrinsic as well as by extrinsic mechanisms. The principal extrinsic mechanisms include the sympathetic vasoconstrictor innervation and epinephrine, whereas the roles of the vasodilator gastrointestinal and pancreatic hormones, and autacoids released from the gastrointestinal tract, remain to be established convincingly. Intrahepatic portal vascular resistance is not significantly controlled by intrinsic mechanisms, and responses to extrinsic mechanisms may be directed principally toward maintenance of portal venous pressure. Two aspects of liver blood flow are discussed in particular detail. First, hormones or drug introduced into one inflow to the liver (e.g., the portal vein) alter the vascular resistance not only of that circuit, but also of the other inflow circuit (hepatic arterial) by a transhepatic mechanism that does not depend on recirculation of the hormone or drug. Second, glucagon, but not other polypeptide vasodilator hormones, prevents hepatic arterial vasoconstriction due to stimuli that include sympathetic nerve activation. This effect occurs at portal or arterial glucagon concentrations close to the pathophysiological range.

Animals↗
PubMed1986

Intrahepatic circulation in liver disease.

Using the multiple indicator dilution approach, events occurring in the microvascular bed can be characterized in experimental animals with different types of cirrhosis and in man. Intrahepatic shunts can be found shunting blood away from sinusoids in both cirrhotic patients and cirrhotic animals. Such shunts were present in about one-third of cirrhotic patients with portal hypertension, and occurred mainly between the portal vein and hepatic veins. In cirrhotics, portohepatic anastomoses are usually large in diameter (more than 20 micron in diameter). Collagenization of the space of Disse and the progressive transformation of sinusoids into capillary-like channels decrease the extravascular space accessible to albumin and probably to other large molecules and protein-bound substances. However, unlike findings obtained in well-capillarized organs, these sinusoidal changes do not appear to limit the diffusion of sucrose, water, and lipophilic substances, such as lidocaine in the extravascular and intracellular spaces. The pattern observed for labeled sucrose curves following hepatic artery injection in cirrhotic patients could be secondary to the passage through the dense peribiliary capillary plexus originating from the enlarged arterial bed in cirrhosis. The difference in the perfusion of cirrhotic nodules with regard to the portal venous and hepatic artery routes introduces important new concepts in the overall mechanism of the elimination of endogenous and exogenous substances by the cirrhotic liver: blood entering the liver by the two afferent vessels will not flow through the same vascular bed before reaching the efferent hepatic veins.

Animals↗
PubMed1989

[Evaluation of disorders of portal and total hepatic blood flow in patients with chronic diffuse liver diseases].

The total hepatic blood flow measured with radioactive colloidal gold and the portal blood flow with the echo-Doppler method were investigated in 19 healthy examinees and 63 patients with chronic diffuse liver diseases. In the group of healthy examinees, the average values of the total hepatic blood flow was 1254 +/- 231 ml/min and of the portal one 1104 +/- 227 ml/min. The lowest blood flow values were obtained in patients with decompensated cirrhosis, especially in the hepatic (704 +/- 186 ml/min) and the portal blood flow (562 +/- 198 ml/min). In all the groups of examinees, registered values of the total hepatic blood flow were significantly higher than the values of the portal blood flow. The relations of the values obtained by both methods, among groups, were similar. By both methods decreased values are not obtained in liver steatosis and chronic persistent hepatitis in relation to the normal values. In patients with more serious forms of chronic diffuse liver diseases (cirrhosis and chronic active hepatitis) significantly lower blood flow values than the normal ones were obtained. Both methods contribute to the investigation of liver circulation disturbances, liver function damages, and to the follow-up of the liver disease course. The possibility of an indirect evaluation of the arterial hepatic blood flow from the difference of hepatic and portal blood flows may mean a new approach to the investigation of pathophysiological liver occurrences.

Adult↗
PubMed1983

The liver and circulating thyroid hormones.

The liver plays a major role in modifying the total circulating hormone concentrations of thyroxine and triiodothyronine by secretion and degradation of carrier proteins. It also is a major site of peripheral conversion, degradation, and excretion of thyroid hormones. We review the liver's role in thyroid hormone physiology and summarize the changes in circulating thyroid hormone concentrations in various liver diseases.

Carcinoma, Hepatocellular↗