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At least 73 records · Page 4Linked to original sources
PubMed2004

Nodular lesions associated with abnormal liver circulation.

In order to present new findings of imaging studies and pathology, we describe nontypical lesions rather than well-known typical lesions such as focal nodular hyperplasia (FNH), hepatocellular adenoma, nodular regenerative hyperplasia (NRH) and large regenerative nodules in liver with idiopathic portal hypertension (IPH). Nontypical lesions are not definitively diagnosed as any of the above typical well-known lesions. These lesions are not rare, and are clinically important since they must be differentiated from hepatocellular carcinoma. These lesions can be formed by hyperperfusion of either the artery or the portal vein. They are found in either the hilar area or peripheral area. The extranodular liver (background liver) shows various histological findings, being nearly normal in some cases but showing a clearly abnormal vasculature in others. The lesions, therefore, present various patterns in imaging. Pathological examination also shows variation in the size of the lumen of portal veins and arteries. Abnormal arrangement of arteries and portal veins are also demonstrated, while parenchymal nodular liver tissues are uniformly nonneoplastic benign hyperplastic tissues. These nontypical lesions and well-known typical lesions (FNH, NRH and IPH) are explained by a single etiological mechanism of anomaly of the portal tract. They can be collectively called anomalous portal tract syndrome. For their definitive diagnosis, the structure and hemodynamics of the nodules need to be clarified by images. Biopsy is also necessary to confirm that the lesions consist of benign hepatic tissues. Subsequently, these findings should be evaluated comprehensively.

Adolescent↗
PubMed1989

Assessment of liver circulation by quantitative scintiangiography: evaluation of the relative contribution of the hepatic arterial and portal venous blood flows to liver perfusion.

Quantitative hepatic scintiangiography was previously used for evaluating the relative contribution of hepatic arterial and portal venous blood flows to the hepatic circulation. The present study compares 3 different procedures (automatic and manual integration, and slope fitting methods) for analyzing the hepatic time activity curves obtained after bolus i.v. injection of 370 MBq 99mTc-diethylentriaminopentacetic acid. Twenty five subjects were studied: five controls, ten cirrhotics, and ten portal hypertensive patients previously submitted to side to side portacaval anastomosis. The correspondence between results given by the different methods was satisfactory only in shunted patients, and the reproducibility of computed parameters was quite poor for all procedures. Accordingly, none of the methods can be considered as supporting reliable quantitative pathophysiological evaluations. However, the hepatic arterial/portal venous flow ratio was found to be increased in liver cirrhosis and in shunted patients and therefore, in spite of the limitations underlined before and of the absence of data on the reproducibility of consecutive injections, hepatic scintiangiography may be of some clinical utility.

Adult↗
PubMed1995

Role of nitric oxide in porcine liver circulation under normal and endotoxemic conditions.

The role of nitric oxide (NO) in the liver vasculature during baseline and endotoxic shock states was evaluated in 17 anesthetized pigs. Mean systemic arterial pressure, pulmonary arterial pressure, and portal venous pressure and flow, hepatic arterial pressure and flow, and cardiac output were measured. Pressure-flow (P-Q) relationships defined resistances as a back pressure and a slope. Inhibition of nitric oxide synthase (NOS) with NG-nitro-L-arginine methyl ester (L-NAME) at baseline increased mean arterial pressure, pulmonary arterial pressure, hepatic arterial pressure, and the slopes of their P-Q relationships (P < 0.05) but had no effect on portal venous pressure or its P-Q relationship. After endotoxin (10 micrograms/kg iv), NO induced arterial dilation and attenuated increases in portal venous and pulmonary arterial resistances (P < 0.05) that were reversed by L-NAME. NOS inhibition was stereospecifically reversed by L-arginine. Local control of liver blood flow at baseline via the hepatic arterial buffer response and hepatic arterial autoregulation were increased in gain after L-NAME. Endotoxic shock ablated the hepatic arterial buffer response and autoregulation independent of either NO or an alpha-adrenergic-receptor agonist (P < 0.05). Under baseline conditions, NO modulates pulmonary, systemic, and hepatic arterial but not portal venous resistances. NO production during endotoxic shock induces arterial hypotension and hepatic arterial vasodilation and attenuates increases in both portal and pulmonary resistances. NOS inhibition in endotoxic shock could increase morbidity due to a loss of local control of liver blood flow and marked increases in resistance to venous return across both the liver and lungs.

Animals↗