Liver circulation, liver function, and liver integrity.
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Hepatectomy is a complicated operative procedure because of its anatomical complexity, vascular variability, and impaired hepatic function due to associated hepatitis or cirrhosis. Thus preoperative detailed topography and precise liver resection volume measurements should be obtained for a curative hepatectomy. The aim of this study was to assess the feasibility and accuracy of a novel three-dimensional (3D) virtual hepatectomy simulation software in patients who underwent liver resection or living donor liver transplantation. We developed the hepatectomy simulation software, which was programmed to analyze detailed 3D vascular structure and to predict liver resection volume and margins. In 72 patients receiving hepatectomy, the predicted liver resection volumes and margins revealed a significant correlation with the actual value with a mean difference of 9.3 mL (P < .0001) and 1.6 mm (P < .01), respectively. The drainage area by hepatic veins was quantified to achieve reconstruction of the corresponding venous branch. In conclusion, this hepatectomy simulation software reliably predicted an accurate liver resection volume, the cancer-free margin, and the drainage volume of hepatic vein branches. This software may promote curative hepatectomy and may be used for other interventional therapies in the treatment of liver disease.
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The changes of hepatic hemodynamics and hemorrheology were investigated in dogs with acute liver damage induced by acetaminophen. There were remarkable disturbance in liver circulation and hemorrheological abnormality occurring in both slight and severe liver damage. The study indicated that the degree of disturbance in liver circulation as well as in hemorheological change is positively correlated with the severity of liver damage. For example, marked increase in blood viscosity linked with elevated fibrinogen level appeared in slight liver damage, whereas reduced blood viscosity associated with decreased plasma fibrinogen level and hematocrit occurred in severe liver damage. This study also revealed that the increase of portal venous resistance (PVR) and the disturbance of liver circulation in slight liver damage were chiefly related to the increase of blood viscosity and the increase of PVR in severe liver damage was mainly associated with the reduction of the radius of portal vein.
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Liver transplantation is becoming more and more common treatment method of liver diseases. The occurring complications may result from ischemia and reperfusion. However, the precise mechanism of these changes is not fully known. Microcirculation disturbances leading to ischemic damage of cells or their death are among those factors which cause liver damage under the influence of ischemia and reperfusion. These disturbances are intensified by increase of liver ischemia time and correlate with the number of wasted away hepatocytes. Endothelial cells, Browicz-Kupffer cells, neutrophils and thrombocytes are thought to play an essential role in liver microcirculation disturbances. Disturbed balance between local vasodilators and vasoconstrictors is also an important factor as it increases the lesions caused by reperfusion due to improper blood circulation. Nitrogen oxide (NO) is the most important local vasodilator. Inhibition of its synthesis in the period of early liver damage due to reperfusion causes a decrease of blood flow and increase of the occurring changes. Such strong vasoconstrictors as endothelin-1 and thromboxane play an important role. Reperfusion by damaging endothelial cells of sinusoid vessels affects the loss of endothelial barrier by the liver sinusoid vessels.
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Liver hemodynamics is characterized by a dual venous and portal blood supply whose physiologic variations are particularly evident during digestion. In the normal subject portal blood flow is laminar with the left liver receiving the blood from the small intestine while the left liver is supplied by the blood from the spleen and colon. In pathologic conditions increased arterial blood flow accompanies the decreased portal flow. Portal hypertension in its various forms is the most frequent and important circulatory alteration in chronic liver disease; besides the "organic" obstacles to the hepatic blood flow there are the dynamic mechanisms which regulate the vascular resistance in the microcirculation Therapies which impact on liver circulation are surgical, of interventional radiology and medical, used in the prevention and cure of complications of portal hypertension.
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.
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