Three-dimensional observations on the alterations of lobular architecture in chronic hepatitis with special reference to its angioarchitecture for a better understanding of the formal pathogenesis of liver cirrhosis

For a better understanding of the formal pathogenesis of liver cirrhosis, the angioarchitecture of the liver lobule in chronic viral hepatitis was investigated three dimensionally. The histological reconstruction method, using serial histological sections, was adopted for the three-dimensional observation. Histology of the case showed chronic active hepatitis with occasional fibrous bridging of the portal to portal tract or hepatic vein. Graphic reconstructions revealed various degrees of altered angioarchitecture from place to place. While the conducting portion of the portal vein was almost preserved, the pathological changes mostly began at the parenchymal portion, especially second step or subsequent branches of the portal vein. In general, portal vein branches showed damage such as stenoses, disappearance, an increase and decrease in number and distorted spatial arrangements. Even in less damaged portal tracts, portal veins showed such changes to some extent. In severely damaged places with bridging fibrosis, a normal lobular angioarchitecture was completely lost; instead, portal veins, arteries and hepatic veins were tangled with each other. Parenchymal nutrition was suggested to be dependent on the remaining third-step portal branches or newly formed ones. However, the hepatic vein system had a tendency to be preserved and distributed fluently in the parenchyma. The distortion of these portal vessels indicated various degrees of loss of the lobular architecture. In conclusion, it is suggested that an early histological sign of cirrhosis develops in the course of chronic hepatitis.     

Epithelioid hemangioendothelioma with marked liver deformity and secondary Budd–Chiari syndrome: Pathological and radiological correlation

A case of malignant epithelioid hemangioendothelioma of the liver in a 48-year-old woman with severe portal hypertension and marked deformity of the liver is presented. This woman had a history of mild liver dysfunction since the age of 30 years, and abdominal distention, esophageal varices, splenomegaly and ascites since October 1996. Imaging examinations revealed liver deformity with severe atrophy of the left lobe and the anterior segment of the right lobe. Celiac arteriography showed narrowing and upward deviation of the proper hepatic artery, and occlusion of the left and right anterior hepatic arteries. Since March 1997, hepatic venography showed stenosis in the right hepatic vein truncus. Budd-Chiari syndrome was clinically diagnosed. She died in June 1997. The autopsy disclosed massive tumor embolism in the left and right anterior portal branches, few in the hepatic artery, and occlusion of the left and right anterior hepatic arteries. The extensive tumor embolism resulted in portal hypertension, and atrophy of the left lobe. The anterior segment of the right lobe was probably caused by the occlusion of both the hepatic arteries and the portal veins. The posterior segment of the right lobe, without massive tumor embolism in its portal branch, appeared hypertrophic.     

A study of the accessory hepatic vein to segments VI and VII with a morphological reconsideration of the human liver

Introduction The liver is supplied by the common hepatic artery from the celiac trunk and by the portal vein from the gastrointestine. This double blood supply to the liver by the hepatic artery and the portal vein produced a complicated structure in the liver. For the blood outflow, we can see right, intermediate and left hepatic veins, and irregular veins: the accessory hepatic veins. These veins drain the blood in the liver into the inferior vena cava. In this study, we studied the layout of the accessory hepatic vein draining segments 6 and 7 in the human livers and attempted to reconsider the structure of the liver by the layout of the accessory hepatic vein. Methods Sixty livers were subjected in this study. They were prepared by using forceps to trace the layout of the blood vessels inside the livers. We carefully examined the relation between the layouts of the accessory vein to the segments 6 and 7 and of the portal vein. The confluence patterns of the accessory hepatic vein into the inferior vena cava were also examined to find the character of the vein. The relation between the accessory hepatic vein and standard hepatic veins was also studied. Results We found 2.2 accessory hepatic veins in one liver on average in our study. The vein was always within the area of segments 6 and 7, and did not surpass the boundary. We found at most five accessory hepatic veins in a liver in two cases. The accessory hepatic vein to the segments 6 and 7 always had its stem on the dorsal side to the portal vein. Different from the stem, the periphery of the accessory hepatic vein freely distributed with the peripheral branches of the portal vein. The area distributed by the accessory vein was also always dorsal part within the segments 6 and 7. The vein was small usually, but was big in few cases. When the vein was big, the area became solely drained by the accessory vein, because the standard hepatic veins (right and intermediate hepatic veins) did not reach the area, and we did not find any communication between the accessory vein and the standard veins. As the remaining region in the segments 6 and 7 became smaller, the draining right standard hepatic vein became shorter and smaller. Discussion The region drained by the accessory hepatic vein excluded the standard hepatic veins. Therefore, there are two different draining venous networks in the area of segments 6 and 7 classified by Couinaud. Conclusion The accessory hepatic vein draining segments 6 and 7 distributed somewhere dorsal side in the segments 6 and 7. The area where the accessory vein distributed was the region where standard hepatic veins did not reach. This would suggest that the region drained by the accessory hepatic vein makes an isolated segment in the liver in the segments 6 and 7 by the Couinaud’s Classification. The area might have a unique blood circulation system.     

Hepatocellular prolapse of hepatic portal tracts and subendothelial space of central veins in idiopathic portal hypertension

We report a case of idiopathic portal hypertension (IPH) with unusual liver pathology. The liver showed changes similar to these previously reported in IPH and, in addition, we observed the unusual features of prolapse of hepatocytes into portal tracts and also into the subendothelial space of hepatic veins. Hepatocyte prolapse into hepatic veins has previously been reported only in patients with a history of androgenic steroid therapy and immunosuppressive therapy. We speculate that, in our case, prolapse of hepatocytes could be related to the abnormal intrahepatic blood flow or to intrahepatic vasculopathy.     

Simultaneous aberrant left and right gastric veins draining directly into the liver.

Aberrant gastric veins draining directly into the liver are rare variations of the portal vein system. We report on an autopsy in which both right and left gastric veins drained directly into the liver without joining the portal vein. Although the left gastric artery adopted a standard disposition, the left gastric vein was indeed found to ascend from the lesser curvature through the upper part of the lesser omentum. After receiving branches from the gastroesophageal junction, it directly entered the left part of the porta hepatis. The right gastric vein ascended from the lesser gastric curvature along and in front of the right aspect of the common bile duct without ending in the portal vein. It crossed in front of the common hepatic duct and directly entered the porta hepatis. Careful dissection within the liver parenchyma showed that both gastric veins ended in the intra-hepatic part of the left branch of the portal vein. Although aberrant gastric veins are known variations of the portal vein system, the conjunction of both right and left gastric vein has never been reported. It highlights the possibility that the venous drainage of the gastric lesser curvature may be totally independent of the main portal vein.     

A comparative histological and morphometric study of vascular changes in idiopathic portal hypertension and alcoholic fibrosis/cirrhosis

AIM: To examine the pathological changes of hepatic arteries in idiopathic portal hypertension (IPH) which is characterized by the obliteration of the intrahepatic portal vein branches and presinusoidal portal hypertension. METHODS AND RESULTS: Liver specimens (biopsied or surgically resected) from 20 patients with IPH, 20 patients with alcoholic fibrosis/cirrhosis (AF/C) and 20 histologically normal livers were used. The vascular lumina of arterial and venous vessels in portal tracts were morphometrically evaluated by an image analysis system. The ratio of portal venous luminal area to portal tract area (portal venous index) of IPH and that of AF/C were significantly reduced compared with normal liver. The portal venous index for IPH was significantly lower than that for AF/C. The ratio of hepatic arterial luminal area to portal tract area for AF/C was significantly higher than that in normal liver; however, that for IPH was similar to normal. The peribiliary vascular plexus was increased in AF/C but not in IPH. In AF/C, the number of mast cells and macrophages known to be the source of angiogenic substances was significantly increased in the portal tract compared with normal liver, while in IPH it was not increased. CONCLUSIONS: In AF/C, a reduction in portal venous lumen was associated with an increase of hepatic arterial lumen and of angiogenesis-related cells in portal tracts. However, such compensatory arterial changes were not evident in IPH, and this compensatory failure may be a feature of IPH.     

Microvascular anatomy of the non-lobulated liver of adult Xenopus laevis: A scanning electron microscopic study of vascular casts

The microvascular anatomy of the non-lobulated liver of adult Xenopus laevis was studied by scanning electron microscopy of vascular corrosion casts. Hepatic portal veins and hepatic arteries entered hepatic lobes at the hiluses, hepatic veins left at these sites. Intraparenchymal, hepatic portal veins branched up to 10 times before terminal portal venules supplied liver sinusoids. Hepatic arteries closely followed portal vessels. Arteriolar side branches formed anastomoses with close by portal venules (arteriolar-portal anastomoses; APAs), liver sinusoids (arteriolar-sinusoidal anastomoses; ASAs), and peribiliary plexus vessels. Distally, hepatic arteries anastomosed with terminal portal venules having >100 μm in diameter. Liver sinusoids formed a dense three-dimensional network displaying signs of non-sprouting and sprouting angiogenesis evidenced by “holes” and blind ending tapering cast vascular structures (sprouts), respectively. Sinusoids drained via efferent hepatic veins. Right and left hepatic veins drained into the posterior caval vein. Locally, a dense honeycomb-like 3D-meshwork of resin structures was found around terminal portal venules and hepatic arteries. These networks were fed by hepatic arterioles and drained into adjacent terminal portal venules. As their morphologies differed significantly from sinusoids and they were found at sites where diffuse lymphoid tissue is described, we are convinced that they represent the vasculature of diffuse lymphoid tissue areas. Frequencies and diameter ratios of hepatic portal venules versus hepatic arterioles anastomosing with the former (APAs) implicate that the arterial supply contributes to the oxygenation of parenchymal and stromal cells rather than to a significant increase in blood flow towards hepatic sinusoids.     

In the non-cirrhotic stage of nonalcoholic steatohepatitis, angioarchitecture of portal veins and lobular architecture are maintained

The morphogenesis of lobular restructuring to liver cirrhosis in nonalcoholic steatohepatitis (NASH) is yet to be clearly understood. Therefore, we observed tissue samples from three biopsies and one autopsy with NASH in the non-cirrhotic stage three-dimensionally to elucidate the evolution of fibrosis and the changes of angioarchitecture. Histologic reconstructions revealed that pericellular fibrosis developed around the central vein in the early stage and gradually progressed to arch-shaped band-like fibrosis connecting the central veins in the neighboring lobules. In contrast, the basic angioarchitecture of the portal vein in the portal tracts tended to be preserved in the non-cirrhotic stage, although the portal vein architecture was slightly altered as the portal tract underwent gradual fibrous expansion. In addition, a striking development of arteries originating from the portal tract was found in the fibrotic area around the central and sublobular veins. In summary, while central–central bridging fibrosis and ectopic arterial development were conspicuous, the lobular architecture was maintained relatively well in the non-cirrhotic stage of NASH because of only mildly damaged angioarchitecture of the portal veins. The process of lobular restructuring in NASH is considered to be different from that in chronic viral hepatitis in the non-cirrhotic stage.     

Identification of segments VI and VII of the liver based on the ramification patterns of the intrahepatic portal and hepatic veins

We describe the pattern of intrahepatic vessel ramification in the right posterior hepatic sector in a population of 197 adults. Each specimen was dissected from its visceral (inferior) surface in order to demonstrate variations in the distribution of the portal vein branches to the hepatic segments of the right lobe, especially to segments VI (S6) and VII (S7) as described by Couinaud. We also examine whether three hepatic veins, i.e., the right hepatic vein (RHV), middle hepatic vein (MHV), and the short hepatic vein (SHV), aid the identification of segmental portal branches in the lower posterior sector. Four major patterns of branching of the posterior sectorial trunk of the portal vein system are described. In group A (32.0%) a single posterior trunk formed an arch‐like pattern sending multiple branches to S6 and S7 (P6 and P7). We named the multiple branches to the apparent S6 the inferoposterior portal branches. It was difficult to identify which of these branches were equivalent to P6. In group B (27.9%), the posterior sectorial trunk bifurcated to form P6 and P7. In most of the specimens in this group, therefore, we were able clearly to identify both S6 and S7 based on the portal vein system. In group C (6.6%), the trunk trifurcated to form P6, P7, and an intermediate branch, which supplied both segments or a gray zone between them. Group D (33.5%) included variations of the anterior segmental branches, and in specimens of this group, the anteromedial border of the sector was difficult to identify. Notably, the three‐dimensional interdigitating topographical relationship of the hepatic veins and the portal branches was not evident in the lower posterior sector, since tributaries of the RHV and the portal branches followed similar courses and paralleled each other in the region and since the territory of the SHV was usually restricted to the superficial parenchyma near the inferior surface. In group A, tributaries of the RHV/SHV (>3 mm in diameter) passed between the inferoposterior portal branches in only 22.2%/14.3% of the specimens. Thus the hepatic veins often did not reveal which of the multiple inferoposterior branches was P6. Moreover, in the subset of Group B in which the segments were identified based on the portal vein ramification, tributaries of the RHV/SHV (>3 mm in diameter) showed the intersegmental interdigitating arrangement in only 32.0%/6.0% of the specimens. In addition, a thick tributary of the MHV, sometimes arising from S6, did not run along, but penetrated the S5/S6 border plane from the lateral to the medial side. Therefore, the three hepatic veins (RHV, SHV, MHV) often did not aid the identification of the liver segments in the region. Consequently, the less than ideal combinations of irregular configurations of the portal and hepatic venous systems suggest that the right posterior segments cannot be conclusively identified anatomically in 30–40% of cases. Other means of identification, such as the conventional proportional manner (the upper and lower halves of the posterior sector roughly correspond to S6 and S7) may be required. Clin. Anat. 12:229–244, 1999. © 1999 Wiley‐Liss, Inc.     

Right ligamentum teres joining to the right branch of the portal vein

Ligamentum teres joining to the right branch of the portal vein in a 79-year-old Japanese male cadaver was noted during student dissection at Kumamoto University in 2004. The ligamentum teres entered the liver along the left side of the gallbladder fossa. The quadrate lobe was not distinguished from the left lobe in the visceral surface. When the liver parenchyma was removed by tearing off to expose the branches of the portal and hepatic veins, it was clarified that the ligamentum teres unusually joined to the bifurcation of the upper anterior and lower anterior branches of the right branch of the portal vein. The ligamentum teres is the remnant of the umbilical vein working throughout fetal life. Initially a pair of the umbilical veins entered the sinus venosus. During the fourth and fifth weeks they connect to the hepatic sinusoids, which become the portal and hepatic veins, and the parts entering the sinus venosus of both umbilical veins disappear. By the eighth week, as all remainder of the right umbilical vein disappears, the left umbilical vein is the only one to carry blood from the placenta to the liver. It results in the ligamentum teres joining to the left branch of the portal vein. However, in the present case it is thought that the right umbilical vein remained instead of the left one for some reason, and it then became the right ligamentum teres joining to the right branch of the portal vein.     

Vascular Development and Differentiation During Human Liver Organogenesis

The vascular architecture of the human liver is established at the end of a complex embryological history. The hepatic primordium emerges at the 4th week and is in contact with two major venous systems of the fetal circulation: the vitelline veins and the umbilical veins. The fetal architecture of the afferent venous circulation of the liver is acquired between the 4th and the 6th week. At the end of this process, the portal vein is formed from several distinct segments of the vitelline veins; the portal sinus, deriving from the subhepatic intervitelline anastomosis, connects the umbilical vein, which is the predominant vessel of the fetal liver, to the portal system; the ductus venosus connects the portal sinus to the vena cava inferior. At birth, the umbilical vein and the ductus venosus collapse; the portal vein becomes the only afferent vein of the liver. The efferent venous vessels of the liver derive from the vitelline veins and are formed between the 4th and the 6th week. The hepatic artery forms at the 8th week; intrahepatic arterial branches progressively extend from the central to the peripheral areas of the liver between the 10th and the 15th week. Hepatic sinusoids appear very early, as soon as hepatic cords invade the septum transversum at the 4th week. They then progressively acquire their distinctive structural and functional characters, through a multistage process. Vascular development and differentiation during liver organogenesis is, therefore, a unique process; many of the cellular and molecular mechanisms involved remain poorly understood. Anat Rec, 291:614–627, 2008. © 2008 Wiley‐Liss, Inc.     

Beneficial effect of glucocorticosteroids for esophageal varices due to idiopathic portal hypertension following systemic lupus erythematosus]

A 54-year-old female experienced morning stiffness and arthralgia of the hands from November 2001 and consulted her local doctor in January 2002. Hematological data showed liver dysfunction and antinuclear antibody was positive. In February 2002, the patient was admitted to our hospital to investigate these abnormalities of liver function further. The features of arthritis, thrombocytopenia with elevated platelet-associated IgG, positive antinuclear antibody, and anti-DNA antibody lead to a diagnosis of systemic lupus erythematosus. Liver biopsy revealed infiltration of Glisson's capsule by plasma cells, compatible with autoimmune hepatitis. We performed hepatic venography to investigate severe pancytopenia, remarkable splenomegaly and esophageal varices. Wedged hepatic venous pressure was mildly elevated, and hepatic veins displayed sharp angles, smooth walls and development of anastomosis with each other. These findings suggested idiopathic portal hypertension. Cytopenia and liver dysfunction gradually improved on treatment with 40 mg/day prednisolone. Esophageal varices were disappeared, and splenomegaly had improved after 6 months. As autoimmune factors are considered to underlie the development of idiopathic portal hypertension with systemic lupus erythematosus, steroid administration represents a therapeutic option in this condition.     

Expression of HLA-DR antigen on hepatic vascular endothelial cells in idiopathic portal hypertension.

Immunologic abnormalities have been reported in idiopathic portal hypertension, though the exact immunologic mechanism(s) leading to various portal venopathies in this disease remain unsettled. Recently, aberrant expression of HLA-DR antigen on target cells has been noted in the organ-specific autoimmune diseases. In this study the expression of HLA-DR antigen on the hepatic vasculature was surveyed immunohistochemically in idiopathic portal hypertension (n = 36) and in control livers: normal livers (n = 27), chronic active hepatitis (n = 35) and cirrhosis (n = 21). Endothelial cells of hepatic veins and hepatic arteries occasionally expressed HLA-DR antigen, and there was no difference in the expression between idiopathic portal hypertension and controls. Endothelial cells of the main portal vein, within the small and medium-sized portal tract, did not express HLA-DR antigen in idiopathic portal hypertension and controls. By contrast, endothelial cells of the smaller venous radicles, including inlet venules in these portal tracts other than the main portal vein, more frequently expressed HLA-DR antigen in idiopathic portal hypertension (78%) than in chronic active hepatitis (26%), cirrhosis (29%) and normal liver (15%). These data raise the possibility that the smaller venous radicles in the small and medium-sized portal tracts are targets of immunologic attack in idiopathic portal hypertension.     

Idiopathic portal hypertension: a histopathological study of 26 Japanese cases

Analysis of 25 liver biopsy specimens and one autopsy specimen from 26 Japanese patients (23 women and three men) with idiopathic portal hypertension revealed findings that collectively appeared diagnostic for the condition. Changes in the portal tract included capillary dilatation, phlebosclerosis, and fibro-elastosis of the stroma. Many portal veins were dilated and had herniated into the surrounding hepatic parenchyma. Portal vein obliteration and loss of bile ducts were a rare complication. The acinar architecture was disturbed by: 1 capillary and necro-infiammatory bridging, mostly between portal tracts and terminal hepatic veins; 2 the formation of isolated megasinusoids in a random distribution; 3 displaced and abnormally large hepatic vein branches with or without phlebosclerosis and 4 slender, curved fibrous septa (hairline septa). Early nodular regeneration was found in 25% of the cases. Our review supports the contention that incomplete septal cirrhosis may be a late manifestation of idiopathic portal hypertension. It is not clear whether the biopsy findings in Japanese patients differ only in severity from those in western patients, or whether the conditions differ pathogenetically. Some histopathological findings in the Japanese cases, in particular the necroinflammatory changes, are difficult to reconcile with portal hypertension as a primary haemodynamic abn rmality.     

Liver disease in rhesus monkeys infected with simian immunodeficiency virus.

Rhesus monkeys infected with simian immunodeficiency virus (SIV) develop a syndrome very similar to patients with acquired immune deficiency (AIDS), including liver disease. This prospective study was undertaken to define the pathology, course, and pathogenesis of liver disease in 20 rhesus monkeys (Macaca mulatta) after intravenous inoculation with the standardized isolate SIV/DeltaB670. Tissue samples from liver and gallbladder between 2 and 24 weeks after inoculation were examined histologically and immunohistochemically for SIV gag protein p26, and by in situ hybridization with an SIV riboprobe. Histologically there was infiltration of portal tracts and around hepatic veins and venules by mononuclear inflammatory cells, focal bile duct damage, proliferation of bile ductules, and focal lobular inflammation as early as 2 weeks after infection. The severity and extent of these lesions were graded semiquantitatively and showed that bile duct damage and hepatic venulitis were the most significant changes. Simian immunodeficiency virus gag protein p26 and SIV RNA were detected in scattered mononuclear cells in portal tracts and sinusoids, but not in hepatocytes or bile duct epithelial cells. The data indicate that the liver is involved early during the course of SIV infection, followed by persistent changes until the terminal stage of the disease. Our findings suggest that the liver damage in SIV-infected rhesus monkeys is similar to the changes observed previously in AIDS patients.     

The chronic form of the Budd-Chiari syndrome

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.     

Portal vein or hepatic vein? A curious aberrant vasculature in the liver with idiopathic portal hypertension

The existence of aberrant vasculatures has been described as one of the characteristic findings in the liver with idiopathic portal hypertension (IPH). In this paper, the morphological features and the genesis of aberrant vasculatures were studied on the basis of autopsy and biopsy materials of IPH and animal experiments. Aberrant vasculatures in IPH livers are characterized as thin-walled vessels located mainly adjacent to the portal tracts and at times in the hepatic lobules. Although some of them are morphologically very similar to hepatic vein branches, they are portal in nature. These aberrant vessels develop in order to compensate for portal circulatory insufficiency due to obliteration of portal vein branches, and play an important role in maintaining an adequate blood supply to the parenchyma. It is predicted that decrease of these intrahepatic collateral vessels is responsible for or related to parenchymal atrophy and deterioration of liver function in the advanced stage of this disease. We regard these vasculatures as characteristic of the intrahepatic portal venous obstruction, particularly with portal hypertension accompanied by increased portal blood flow.     

Histological study of intrahepatic cavernous transformation in a patient with primary myelofibrosis and portal venous thrombosis

Summary Cavernous transformation in the liver was examined histologically by serial section observations, in an autopsy case of portal venous thrombosis and primary myelofibrosis. Cavernous transformation was present from the hepatic hilus to medium-sized portal tracts and was composed of dilated and thin-walled vessels. Serial sections disclosed that these vascular channels were anastomotic and occasionally communicated with occluded portal venous radicles. In places they entered directly into the hepatic parenchyma without accompanying biliary or arterial elements, and also drained into the patent portal venous branches beyond the occluded segment. The study demonstrated that cavernous transformation in the liver develops as hepatopetal collaterals secondary to the portal venous obstruction. Periportal and peribiliary capillary plexus may become cavernous in the presence of portal venous occlusion.     

Anatomy of the portal branches and the hepatic veins in the caudate lobe of the liver

The objective of this study was to analyze the caudate portal branches and their relationships with the hepatic caudate veins and propose a new nomenclature for the caudate branches based on their territory of distribution. We realized the fine dissection of the veins of the caudate lobe in 40 human livers fixed and preserved in formalin. In 15/40 (37.5%) cases there was a single branch to the caudate lobe. In 25/40 (62.5%) cases there was more than one branch, with a posterior caudate branch in 20/40 (50%) cases, an anterior caudate branch in 15/40 (37.5%) cases, a left caudate branch in 14/40 (35%) cases, and a right caudate branch in 8/40 (20%) cases. The most frequent combination detected (11/40, 27.5% of cases) was that of the posterior and anterior branches. The venous drainage of the caudate lobe and its papillary process was provided by the superior caudate hepatic vein in 23/40 (57.5%) cases, by the middle caudate vein in 35/40 (87.5%) cases (which was the only vein in 12/35 cases), and by the inferior caudate vein in 16/40 (40%) cases. In 11/40 (12.5%) cases there were accessory caudate veins, which emptied into the left and intermediate hepatic veins. The portal branches and the hepatic veins related to the caudate process were studied. In conclusion, the new nomenclature analyzes more precisely the distribution of the caudate portal branches.     

与LC术有关的胆囊动脉解剖

目的：为临床ＬＣ术提供形态学资料。方法：随机选用３０例肝脏标本,经胆囊动脉及门静脉右支注入乳胶后,在６倍大视场显微镜下观察胆囊动脉的起源、行程、及其与肝脏的关系。结果：据胆囊动脉深、浅支行径的不同,将其分为５种类型。其深支可发出肝支和胆囊支,分别供应肝脏和胆囊;并特别对肝支进入胆囊窝的部位进行了观察和统计。胆囊静脉从胆囊窝底注入门静脉右支,而部分门静脉右支位置表浅,参与组成了胆囊床。结论：处理胆囊窝时,尤应重视胆囊动脉肝支和位置表浅的门静脉右支的存在,以防止出血。