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Portal Inflow (portal + inflow)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Portal-systemic shunting in patients with fibrosis or cirrhosis due to chronic hepatitis C: the minimal model for measuring cholate clearances and shunt

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2007
G. T. EVERSON
Summary Background, Measurement of portal inflow and portal-systemic shunt using cholate clearances could be useful in monitoring patients with liver disease. Aim, To examine relationships of cholate clearances and shunt to cirrhosis and varices and to define minimal sampling requirements. Methods, Five hundred forty-eight studies were performed in 282 patients enrolled in the Hepatitis C Antiviral Long-term Treatment to prevent Cirrhosis (HALT-C) trial. Stable, non-radioactive isotopes of cholate were administered intravenously and orally, clearances (Cliv and Cloral) were calculated from [dose/area under curve (AUC)] and cholate shunt from [(AUCoral:AUCiv) x (Doseiv:Doseoral) x 100%]. Results, Cholate Cloral and cholate shunt correlated with prevalences of both cirrhosis and varices (P < 0.0001 for all). Peripheral venous sampling at 5, 20, 45, 60 and 90 min defined the minimal model. Linear regression of cholate shunt determined from five points within 90 min vs. the standard method of 14 points over 3 h yielded slope of 1.0 and intercept 0.5% (r2 = 0.98, P < 0.0001). Results were identical in the 189 validation studies (slope 1.0, intercept 0.5%, r2 = 0.99, P < 0.0001). Conclusions, Cholate Cloral and cholate shunt may be useful in monitoring patients with liver disease. The 5-point model enhances application of cholate Cloral and cholate shunt in the non-invasive assessment of the portal circulation. [source]

Liver retransplantation in an infant requiring cavoportal hemi transposition

PEDIATRIC TRANSPLANTATION, Issue 4 2004
Deborah Verran
Abstract:, Historically inability to achieve portal inflow to the liver allograft operatively was felt to be a contraindication to orthotopic liver transplantation (OLTx). Cavoportal hemi transposition has been utilized more recently in adult OLTx recipients but rarely in pediatric recipients. Here we report the case of a 10-month-old male with biliary atresia, who required urgent retransplantation with an in situ split cadaver donor allograft for failure of his first liver allograft from portal vein thrombosis. At the time of retransplantation, cavoportal hemi transposition was required to effect portal vein inflow to the allograft because of extensive thrombosis of the recipients portomesenteric venous system. [source]

Successful Living Donor Liver Transplantation in Portomesenteric Thrombosis

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2010
S. G. Iyer
Chronic portal vein thrombosis (PVT) is often considered a relative contraindication for living donor liver transplantation due to the risks involved and higher morbidity. In this report, we describe a surgical strategy for living donor liver transplant in patient with complete PVT using venovenous bypass from the inferior mesenteric vein (IMV) and then using a jump graft from the IMV for portal inflow into the graft. IMV is a potential source for portal inflow in orthotopic liver transplant. [source]

In vivo evaluation of an implantable portal pump system for augmenting liver perfusion

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2000
L. R. Jiao
Background Increasing portal inflow in cirrhosis using a mechanical pump reduces portal venous pressure and improves liver function. A pump has been developed for portal vein implantation in human cirrhosis. This study describes the initial in vivo evaluation in a porcine model. Methods Five Large White pigs underwent laparotomy and exposure of the liver. Flow in the hepatic artery, portal vein and hepatic microcirculation was monitored continuously. Hepatic tissue oxygenation was measured by near-infrared spectroscopy. After baseline measurements the pump was inserted into the portal vein. Pump flow rate was then increased stepwise to 50 per cent over the baseline value for a period of 2 h. The pump was then stopped for 20 min and left in situ while continuing to collect systemic and hepatic haemodynamic data. The animal was killed and biopsies for histological examination were taken from the liver, small intestine and spleen. Results The baseline total hepatic blood flow was 626(39) ml/min; the hepatic artery supplied 18·4(2·1) per cent and the portal vein 81·6(2·1) per cent. The pump was inserted successfully in all animals without surgical complications. During surgical insertion of the pump, the temporary portal vein occlusion resulted in a significant rise in hepatic artery blood flow (22(3) per cent; P < 0·01 versus baseline). Portal vein flow was augmented by pumping; there was a significant correlation between the pump motor speed and portal vein flow (P < 0·0001). This inflow correlated directly with flow in the hepatic microcirculation and hepatic tissue oxygenation (P < 0·001). The pump ran satisfactorily throughout the study. Histological examination revealed no evidence of structural damage to the liver or ischaemic changes in the small intestine or spleen. Conclusion It is technically possible and safe to insert an implantable pump in the portal vein. Portal venous blood flow can be increased up to 50 per cent with a resultant increase in flow in the hepatic microcirculation and hepatic oxygenation and without adverse effects on either hepatic or systemic haemodynamics. © 2000 British Journal of Surgery Society Ltd [source]

Hepatic venous outflow reconstruction in adult living donor liver transplants without portal hypertension

CLINICAL TRANSPLANTATION, Issue 2 2004
Diego Bogetti
Abstract:, Graft congestion is one of the causes of poor graft function in segmental liver transplantation. Three factors are implicated in segmental graft congestion: graft size, hepatic venous outflow and portal inflow. The graft size must be matched to the body weight, which is conventionally done by using graft to body weight ratio. Hepatic blood outflow must be optimized by hepatic vein reconstruction, which can be complicated. High portal blood flow has been shown to be detrimental to small-for-size grafts. These factors are strictly connected to each other. They can all contribute to graft congestion and poor function, while one factor can compensate for the others and decrease congestion. Ideally, all the accessory veins should be reconstructed, if possible, to maximize the outflow. In the absence of portal hypertension and with an adequate sized graft, complex venous reconstruction may not be necessary. We present a case report of an adult living donor liver transplant with the favorable conditions of normal portal pressure and a large sized graft, but complicated by the presence of several accessory hepatic veins. A simple hepatic vein anastomosis was sufficient for adequate outflow and prompt graft function. [source]

Impairment of Hepatic Microcirculation in Fatty Liver

MICROCIRCULATION, Issue 6 2003
SAMIA IJAZ
ABSTRACT Fatty liver or hepatic steatosis, which is the result of the abnormal accumulation of triacylglycerol within the cytoplasm of hepatocytes, is a common histological finding in human liver biopsy specimens that is attributed to the effects of alcohol excess, obesity, diabetes, or drugs. There is a general consensus that fatty liver compromises hepatic microcirculation, the common exchange network upon which hepatic arterial and portal inflows converge, regardless of underlying etiology. A significant reduction in hepatic microcirculation has been observed in human fatty donor livers and in experimental models of hepatic steatosis. There is an inverse correlation between the degree of fat infiltration and both total hepatic blood flow and flow in microcirculation. Fatty accumulation in the cytoplasm of the hepatocytes is associated with an increase in the cell volume that reduces the size of the hepatic sinusoid space by 50% compared with a normal liver and may result in partial or complete obstruction of the hepatic sinusoid space. As a result of impaired hepatic microcirculation, the hepatocytes of the fatty liver have reduced tolerance against ischemia-reperfusion injury, which affects about 25% of the donors for liver transplantation because severe steatosis is associated with a high risk of primary nonfunction after liver transplantation. [source]