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PubMedDate not supplied

Liver volume in patients with or without chronic liver diseases.

BACKGROUND/AIMS: The size of the liver is an important clinical parameter; the aim of this study is to examine the correlation between liver volume and etiology and the severity of disease, and to evaluate its usefulness in predicting survival. METHODOLOGY: Patients observed in this study were comprised of thirty three patients with non-liver disease and 44 patients with chronic liver disease (alcoholic hepatitis, 9; hepatitis B, 24; and hepatitis C, 11). The liver volume was measured from digitized CT scan images. Techniques of planimetry and summation of areas were utilized for calculation. RESULTS: The prediction model to estimate liver volume in patients without liver disease was: liver volume (ml)= [13 x height (cm)] +[12 x weight (Kg)] - 1530. The volume ratio (%) [(volume from reconstructed image /predicted volume) x 100] of alcoholic patients was 135.9+/-25.8, which was significantly higher than that of chronic hepatitis B (73.6+/-15.4) and chronic hepatitis C (74.5+/-20.7). Patients with chronic viral hepatitis were classified into Child-Pugh class A (N=10), B (N=14) and C (N=11). Analysis of variance and trend test revealed that the volume ratio had a significant decreasing trend from the control group (100.5+/-8.1), class A (83.4+/-13.9), class B (72.2+/-13.2) to class C (63.3+/-14.4). CONCLUSIONS: Liver volume can be predicted from patients' weight and height if they have no liver disease. The liver volume ratio correlates much better with etiology and severity of the disease and is a reliable predictor for patient's survival.

Adult↗
PubMed1998

Comparison of liver progenitor cells in human atypical ductular reactions with those seen in experimental models of liver injury.

The ultrastructural characteristics of liver progenitor cell types of human atypical ductular reactions seen in chronic cholestasis, in regenerating human liver after submassive necrosis, in alcoholic liver disease, and in focal nodular hyperplasia are compared with liver progenitor cell types seen during experimental cholangiocarcinogenesis in hamsters; during hepatocarcinogenesis in rats; and in response to periportal liver injury induced by allyl alcohol in rats. Three types of progenitor cells have been identified in human atypical ductular reactions: type I: primitive, has an oval shape, marginal chromatin, few cellular organelles, rare tonofilaments, and forms desmosomal junctions with adjacent liver cells; type II: bile duct-like, is located within ducts, has few organelles, and forms lateral membrane interdigitations with other duct-like cells; and type III: hepatocyte-like, is located in hepatic cords, forms a bile canaliculus, has tight junctions with other hepatocyte-like cells, prominent mitochondria and rough endoplasmic reticulum, and some have lysosomes and a poorly developed Golgi apparatus. Each type is seen during cholangiocarcinogenesis in hamsters, but the most prominent cell type is type II, duct-like. A more primitive cell type ("type 0 cell"), as well as type I cells, are seen in the intraportal zone of the liver within 1 to 2 days after carcinogen exposure or periportal injury in the rat, but both type II and type III are seen later as the progenitor cells expand into the liver lobule. After allyl alcohol injury, type 0 cells precede the appearance of type I and type III cells, but most of the cells that span the periportal necrotic zone are type III hepatocyte-like cells showing different degrees of hepatocytic differentiation. Some type II cells are also seen, but these are essentially limited to ducts. It is concluded that there is a primitive stem cell type in the liver (type 0) that may differentiate directly into type I and then into type II, duct-like or or type III hepatocyte-like cells. The terms oval cell, transitional hepatocyte, biliary hepatocyte, hepatocyte-like cell, atypical ductular cell, neocholangiole, etc., are used to describe these cells. Although these terms are useful as general descriptive terms for liver precursor cells at the light microscopic level, the cells included in these descriptive categories may be very different from one another biologically and ultrastructurally.

Animals↗
PubMed1998

Endothelin 1 aggravates acute liver injury in perfused livers of rats after treatment with D-galactosamine.

The effects of endothelin 1 (ET-1) on hemodynamics and acute liver damage were studied using perfused livers of rats treated with D-galactosamine. In control liver perfused in situ with constant pressure, infusion of ET-1 into the portal vein at a concentration of 0.1 nmol/L decreased the flow rate without a significant leakage of lactate dehydrogenase (LDH) or aspartate transaminase (AST) into the effluent. In contrast, in similarly perfused liver 24 hours after treatment with D-galactosamine (800 mg/kg intraperitoneally), ET-1 caused rapid and remarkable increases in the leakage of LDH and AST from the liver accompanied by the reduction of perfusion flow to the extent similar to that observed in control livers. In addition, ET-1 decreased oxygen uptake and bile secretion in galactosamine-treated livers. The potentiating effects of ET-1 on enzyme leakage were also observed under constant flow conditions. Moreover, infusion of the thromboxane A2 analogue at a concentration of 10 nmol/L decreased the flow rate markedly, yet the rapid increases in enzyme leakage were not observed. Infusion of ET-3 induced the responses of flow reduction and the potentiation of rapid enzyme leakage similar to those obtained with ET-1. Neither the endothelin A-receptor antagonist BQ485 nor the endothelin B-receptor antagonist BQ788 could inhibit the acute liver damage caused by ET-1; instead they exaggerated its effects. The combination of both antagonists together, however, almost completely suppressed the flow reduction and the potentiation of enzyme leakage caused by ET-1. These results indicate that ET-1 is capable of aggravating acute liver damage not merely through reduction of the flow rate but through direct action on liver cells. They also suggest that both the endothelin A and endothelin B receptors are involved in this action of ET-1.

Acute Disease↗
PubMed1994

An experimental study on the disturbance of liver circulation and the change of hemorrheology in dogs with acute liver damage.

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.

Acetaminophen↗
PubMed2001

Auxiliary partial orthotopic liver transplantation: treatment of acute liver failure in a new rat model.

BACKGROUND AND AIMS: Liver regeneration and functional interaction between native liver and graft after auxiliary partial orthotopic liver transplantation (APOLT) are not entirely understood and, therefore, require an experimental model simulating the clinical features of acute liver failure (ALF) and the surgical technique of APOLT. MATERIALS AND METHODS: ALF was induced by subtotal hepatectomy in 50 Lewis rats (200-250 g). Sham operation (I), ALF without treatment (II), ALF with portocaval shunt for decreasing blood flow of the remnant liver (III), and ALF treated by APOLT (IV) were performed. The auxiliary graft represented a left donor liver lobe which was orthotopically implanted using a microsurgical technique including reconstruction of the graft artery and internal biliary drainage. Operative outcomes, serum chemistry and histopathological findings were examined up to the 14th day. RESULTS: ALF without treatment (groups II and III) led to a small droplet fatty degeneration in the hepatocytes and a significant increase of liver parameters until the death of the animals within the first two postoperative days ( P<0.05). After APOLT (group IV), 80% of the animals survived up to the 14th day, revealing significantly decreased liver parameters ( P<0.05), a well-perfused graft and an up to five times increased native liver size with normal architecture. CONCLUSION: This new rat model simulates the clinical features of an ALF treated by APOLT and is especially interesting for further basic research on the interaction between native liver and auxiliary graft after APOLT.

Animals↗
PubMed1986

Benign bile duct tumours, non-parasitic liver cysts and liver damage in males.

Pathogenetic associations between benign hepatic tumours and liver damage were studied in an autopsy series of 91 males with high incidence of alcoholism. Information on the consumption of alcohol was obtained by interviewing a family member or a close friend of the deceased. The reported use of alcohol correlated well with the increase of fatty and fibrotic changes and with the occurrence of liver cirrhosis, alcoholic hepatitis or pancreatitis. Benign bile duct tumours (bile duct adenomas and von Meyenburg's complexes) (n = 26) were associated with the occurrence of bridging (P less than 0.0005) and periportal (P less than 0.025) fibrosis of the liver and, independently from these, with chronic pancreatitis (P less than 0.05) and with non-parasitic liver cysts (n = 14) (P less than 0.01). The weight of the liver was greater (P less than 0.01) in males with focal nodular hyperplasia (n = 3). Cavernous hemangioma (n = 19) occurred independently of the parameters studied. None of the tumours showed significant correlation to liver cirrhosis, alcoholic hepatitis, fatty liver or diseases of the gallbladder. The results are in line with observations on the reactive nature and connections to fibropolycystic liver disease of benign bile duct tumours in laboratory animals and in man. Their presence in human liver specimens should be taken into account as a sign of liver damage, in this study related to heavy use of alcohol or to chronic inflammation of the pancreas.

Adult↗
PubMed2002

Extracorporeal liver perfusion as hepatic assist in acute liver failure: a review of world experience.

BACKGROUND: There are almost no prospective, controlled and randomized clinical trials comparing different approaches towards hepatic assist. In order to create a basis for comparing the value of the existing different hepatic assist methods this article offers a systematic review of the world experience with allogeneic or xenogeneic extracorporeal liver perfusion (ECLP). METHODS: An Internet-assisted search was conducted in the international literature published from 1964 to 2000. Only articles with a clear description of methodology and outcome of patients were included. For multivariate analysis of variance the general linear method (GLM) procedure was used. Differences within the groups were analyzed by chi-square test. Data of 198 patients were included into the statistical analysis for systematic review. RESULTS: The long-term survival rate (SVR) of these patients was 26%, thus not exceeding published data concerning SVR under standard intensive care. Age below 40 years (P<0.029), coma stage lower than III-IV (P<0.003), total perfusion time over 10 hours (P<0.024), hepatitis B as cause for acute liver failure (ALF) (P<0.05) as well as use of baboon and human livers (P<0.02) were identified as independent positive prognostic markers for improved survival. ECLP as bridging therapy to liver transplantation was successful in 12 of 14 patients. CONCLUSION: ECLP using pig livers did not surpass the success of conventional intensive care treatment. An additional effect of transgenic expression of human regulators of complement regulation in porcine livers has not yet been proven. ECLP with human livers not suitable for liver transplantation might prove effective and practicable for temporary hepatic support. Bridging to liver transplantation by long-term ECLP using porcine and human livers appears to have comparable efficacy as bioartificial support methods.

Acute Disease↗
PubMed1979

Regeneration of human liver after hepatic lobectomy studied by repeated liver scanning and repeated needle biopsy.

Regeneration of the residual lobe of the liver after hepatic lobectomy in humans was studied by repeated liver scanning in seven noncirrhotic and three cirrhotic patients. Each patient was studied for several months during the study which lasted from 1-12 years. Regeneration was apparent in noncirrhotic liver remnants following hepatic lobectomy. In the case of a long standing, space occupying lesions such as benign giant cysts, the liver remnant would complete its regeneration process rather early, usually within a few months of hepatic lobectomy. In hepatoma cases, however, regeneration of the residual lobe after hepatic resection usually took five or six months for completion. On the contrary, no definite increase in the size of the liver remnant was seen on repeated liver scanning in cirrhotic patients. Histologic study of the residual lobe was repeated on needle biopsy specimens in two noncirrhotic and four cirrhotic patients. Regenerative hyperplasia of liver cells with large hyperchromatic, or double nuclei never seen in the preresection liver appeared in the liver remnant five, 11, and 27 days after hepatic lobectomy in noncirrhotic patients. In cirrhotics, however, there were no histologic changes between the preresection liver and the postresection remnant studied three, five, 15, 40 days or even two years and 8 months after hepatic lobectomy.

Biopsy, Needle↗
PubMed1999

Risk of major liver resection in patients with underlying chronic liver disease: a reappraisal.

OBJECTIVE: To explore the relation of patient age, status of liver parenchyma, presence of markers of active hepatitis, and blood loss to subsequent death and complications in patients undergoing a similar major hepatectomy for the same disease using a standardized technique. SUMMARY BACKGROUND DATA: Major liver resection carries a high risk of postoperative liver failure in patients with chronic liver disease. However, this underlying liver disease may comprise a wide range of pathologic changes that have, in the past, not been well defined. METHODS: The nontumorous liver of 55 patients undergoing a right hepatectomy for hepatocellular carcinoma was classified according to a semiquantitative grading of fibrosis. The authors analyzed the influence of this pathologic feature and of other preoperative variables on the risk of postoperative death and complications. RESULTS: Serum bilirubin and prothrombin time increased on postoperative day 1, and their speed of recovery was influenced by the severity of fibrosis. Incidence of death from liver failure was 32% in patients with grade 4 fibrosis (cirrhosis) and 0% in patients with grade 0 to 3 fibrosis. The preoperative serum aspartate transaminase (ASAT) level ranged from 68 to 207 IU/l in patients with cirrhosis who died, compared with 20 to 62 in patients with cirrhosis who survived. CONCLUSION: A major liver resection such as a right hepatectomy may be safely performed in patients with underlying liver disease, provided no additional risk factors are present. Patients with a preoperative increase in ASAT should undergo a liver biopsy to rule out the presence of grade 4 fibrosis, which should contraindicate this resection.

Aged↗
PubMed2003

The role of liver biopsy in the management of patients with liver disease.

The role of liver biopsy in the diagnosis and management of liver disease is a controversial issue even among hepatologists. Although most causes of elevated liver enzymes can be determined, or at least suspected, on the basis of a careful history and laboratory tests, histological assessment remains the gold standard for most liver diseases. Histological evaluation can either confirm or refute clinical diagnoses and can provide information about the severity and stage of disease. Occasionally, the liver biopsy also provides an additional diagnosis. The spectrum of nonalcoholic fatty liver disease accounts for a substantial proportion of cases of chronically elevated liver enzymes and can be reliably diagnosed only by liver biopsy. Prognostic information can be obtained in patients with this disorder, as well as in those with alcoholic liver disease and viral hepatitis, and liver biopsy can be used as a guide to their management.

Biopsy, Needle↗
PubMed2006

Cryopreserved fetal liver cell transplants support the chronic failing liver in rats with CCl4-induced cirrhosis.

Hepatocyte transplantation is a promising method for supporting hepatic function in a broad spectrum of liver diseases. The aim of this work was to test the efficacy of human fetal liver cells to support the chronic failing liver in an experimental model of carbon tetrachloride (CCl4)-induced cirrhosis in rats. Liver cirrhosis was induced by intraperitoneal administration of CCl4 at a dose of 0.2 ml (50% v/v solution)/100 g body weight, twice a week for 3 months in rats. Ten days after stopping CCl4 administration (experimental day 0), rats received intrasplenic injection of cryopreserved fetal liver cells (FLC, 1 x 10(7) cells in 0.3 ml medium). As a cirrhotic control group, CCl4-induced cirrhotic rats were used with intrasplenic injection of an equal volume of medium alone. Animals were sacrificed on experimental day 15. Human fetal liver cell transplantation almost completely prevented the death of cirrhotic animals during the 2 weeks after treatment, while high ongoing mortality was seen in the cirrhotic control group. Cell transplantation into the spleen normalized total bilirubin and TBARSs levels and increased albumin levels in blood serum, as well as restoring mitochondrial function and liver detoxification function (assessed by cytochrome P450 contents and activity) compared with the activities seen in the cirrhosis control group. In parallel with this restoration of biochemical and functional liver indices, morphological patterns of liver recovery or regeneration after liver cell transplantation were demonstrated in day 15 samples by light microscopy. These were absent in the group that had received only medium alone.

Animals↗
PubMed1986

[Hepatic GOT and GPT activities in patients with various liver diseases--especially alcoholic liver disease].

GOT and GPT activities were measured in percutaneous needle biopsy specimens of human liver tissue from 98 cases including normal subjects and patients with various liver diseases. Hepatic GOT activity was markedly decreased in liver tissue of patients with nonalcoholic liver cirrhosis. Hepatic GPT activity was markedly decreased in liver tissue of patients with alcoholic liver cirrhosis. The GOT/GPT ratio in liver tissue was increased in patients with alcoholic liver cirrhosis (5.32 +/- 2.03) and alcoholic liver disease (4.78 +/- 2.43). The increased SGOT/SGPT ratio in patients with alcoholic liver disease is due to primarily to the increased LGOT/LGPT ratio.

Alanine Transaminase↗
PubMed1995

Expression of cell adhesion molecules on liver-associated lymphocytes and their ligands on sinusoidal lining cells in patients with benign or malignant liver disease.

Liver sinusoids, in contrast with the capillaries of other tissues, contain large numbers of sequestered lymphocytes. These blood-borne cells preferentially home in the liver. The mechanism regulating the recruitment of these cells and molecular regulation of the recognition of endothelial cells is as yet unclear. The present study sought to evaluate the cell adhesion molecules on human liver-associated lymphocytes and their ligands on sinusoidal lining cells in 29 patients undergoing partial hepatectomy for liver tumors. Liver-associated lymphocytes and peripheral blood lymphocytes were analyzed by flow cytometry using monoclonal antibodies. Frozen sections of liver tissue were stained according to alkaline phosphatase anti-alkaline phosphatase method. Cytometric analysis showed that virtually all liver-associated lymphocytes expressed on their surface the cell adhesion molecules LFA-1 and VLA-4. This liver-associated lymphocyte population also presented a significantly higher percentage of Mac 1, ICAM-1, and LFA-3 and an increased surface expression of LFA-1, LFA-2, and NCAM in comparison with peripheral blood lymphocytes. It was likewise shown that sinusoidal cells express ICAM-1, ICAM-2, ICAM-3, VCAM-1 and LFA-3 ligands. Liver-associated lymphocytes thus strongly express a number of different adhesion molecules. The corresponding ligands were also detected on sinusoidal lining cells. LFA-1 and VLA-4 would seem to be important pathways of temporary lymphocyte-endothelial adhesion in liver sinusoids.

Adenoma↗
PubMed1994

Effect of dietary hyperlipidemic components and fish oil on concentration of lipids in liver and liver fatty acid profile of rats.

This investigation was attempted to clarify the effects of dietary hyperlipidemic components and fish oil on concentration of lipids in liver and liver fatty acid profile of rats. In a first experiment male Sprague-Dawley rats were maintained on a semipurified low-fat diet with 6.5% coconut oil and 1.5% safflower oil, but without added cholesterol, or a high-fat hyperlipidemic diet supplemented with 7.3% coconut oil, 7.3% beef tallow, 0.4% safflower oil, and 1.5% cholesterol for 28 days. Rats fed the hyperlipidemic diet were then switched to fish oil diets with 1.4%, 2.8%, and 5.6% fish oil in exchange for coconut oil and beef tallow for, respectively, 10 and 20 days. In a second experiment male Sprague-Dawley rats were fed low-fat or high-fat diets without or with 1.5% added cholesterol for 28 days. Half of each group was then changed to a fish oil diet (for 20 days) which contained 5.6% fish oil in exchange for coconut oil and beef tallow. In experiment 1, rats fed the hyperlipidemic diet had enlarged fatty livers within 28 days. Experiment 2 showed that cholesterol in the diet was responsible for the accumulating liver lipids. Feeding diets with added cholesterol, the proportions of saturated fatty acids (SFA), especially 18:0, were markedly reduced in liver, whereas levels of monounsaturated fatty acids (MUFA) were greatly increased compared to diets without added cholesterol. This increase was most pronounced with respect to 16:1 and 18:1. In contrast, fish oil diets lowered MUFA level in liver in spite of its high MUFA content. Rats fed the highly saturated hyperlipidemic diet low in 18:2 n-6 had reduced 18:2 n-6 levels in liver compared to rats fed the low-fat diet without added cholesterol. Also, 20:4 n-6 level in liver was markedly reduced after the administration of the hyperlipidemic diet or the fish oil diets. Results of experiment 2 elucidate that cholesterol as well as fish oil sharply lowered 20:4 n-6 level in liver, which might be due to a reduced desaturation. In both experiments feeding fish oil increased all long-chain n-3 polyunsaturated fatty acids (PUFA) in liver. This occurred in a dose-dependent fashion and reached a maximum level with 5.6% fish oil in the diet. When additional cholesterol was applied 22:6 n-3 level in liver fell. This indicates also an impaired desaturation of PUFA due to dietary cholesterol.

Animals↗
PubMed2005

Regional delivery of model compounds and 5-Fluorouracil to the liver by their application to the liver surface in rats: its implication for clinical use.

PURPOSE: The purpose of this study was to examine drug distribution in the liver after drug application to the rat liver surface. METHODS: Phenolsulfonphthalein (PSP) and fluorescein isothiocyanate dextran (MW 4400, FD-4) as model compounds or 5-fluorouracil (5-FU) was applied to the rat liver surface by employing a cylindrical diffusion cell (i.d. 9 mm, 0.64 cm2). Then, blood and the remaining solution in the diffusion cell were collected at selected times, followed by excision of the liver. The excised liver was divided into three sites: the region under the diffusion cell attachment site (site 1), the applied lobe except for site 1 (site 2), and non-applied lobes (site 3). RESULTS: In the case of i.v. administration, there were no differences in PSP concentrations among the three sites of the rat liver, and the concentrations rapidly decreased. On the other hand, the PSP concentration in site 1 after application to the rat liver surface was considerably higher than in site 2 and site 3. In addition, the area under the curve (AUC) value (AUCsite1), calculated from the PSP concentration profile in site 1, was about 10 times larger than that in site 3. A similar trend of regional delivery advantage by liver surface application was observed in the case of the macromolecule model FD-4, with a marked AUCsite1 of about 5 times larger than the other two sites. Moreover, we clarified that the anticancer drug 5-FU preferentially distributed in site 1 after application to the rat liver surface. CONCLUSION: These results demonstrate the possibility of regional delivery of drugs to the liver by application to the liver surface.

Absorption↗
PubMed1993

Purification of macaque liver flavin-containing monooxygenase: a form of the enzyme related immunochemically to an isozyme expressed selectively in adult human liver.

A microsomal flavin-containing monooxygenase (FMO) was purified 77-fold from macacque liver microsomes on the basis of its methyl p-tolyl sulfoxidase activity. Sequential chromatography on anion- and cation-exchangers, lauryl-Sepharose and 2',5'-ADP-Sepharose provided a purified preparation which exhibited an apparent molecular mass of 59 kDa and a pI of 8.3. N-terminal amino-acid sequencing revealed the characteristic Gly-X-Gly-X-X-Gly consensus sequence for the putative FAD-binding domain of microsomal FMO. In marked contrast to the well-characterized hepatic and pulmonary forms present in experimental animals, the macacque liver enzyme displayed stereoselectivity for sulfoxidation of p-tolyl methyl sulfide on the pro-S rather than the pro-R face of the substrate. Polyclonal antibodies raised against the macacque liver form exhibited little or no cross-reactivity with major purified forms of the enzyme isolated from rabbit liver, guinea-pig liver or rabbit lung. Anti-macacque liver FMO did not cross-react with human fetal liver or adult kidney microsomes, but did recognize a 59 kDa constituent of human adult liver microsomes. The intensity of this immunoreactive 59 kDa band correlated well with human liver microsomal N,N-dimethylaniline N-oxygenase activity. We conclude that human adult liver selectively expresses a microsomal FMO which is functionally and immunochemically distinct from the FMO form(s) present in human fetal liver and adult kidney, and from the major hepatic and pulmonary forms present in common laboratory animals.

Adult↗
PubMed1984

Lack of initiating or promoting activity of six benzodiazepine tranquilizers in rat liver limited bioassays monitored by histopathology and assay of liver and plasma enzymes.

Six benzodiazepine tranquilizers were tested in limited in vivo bioassays for their ability to initiate or promote the development of preneoplastic and neoplastic rat liver lesions. The benzodiazepine produced no liver altered hepatocellular foci during a 14-week period of administration whereas a large number were produced by the liver carcinogen, N-2-fluorenylacetamide. To assay for promoting activity and confirm the lack of initiating activity, N-2-fluorenylacetamide was used to produce altered foci and early neoplastic nodules in rat liver by 8 weeks of dietary administration and the benzodiazepines were then administered for 12 weeks. The liver neoplasm promoter phenobarbital had a substantial enhancing effect upon the persistence of early lesions but none of the benzodiazepines showed a similar effect. Thus in these limited bioassays monitored by histopathology, the benzodiazepine tranquilizers failed to exhibit either an initiating or a promoting action. In these studies, the liver and plasma enzymes, glutamate-pyruvate transaminase, glutamate-oxalacetic transaminase, lactic dehydrogenase, alkaline phosphatases, and gamma-glutamyltranspeptidase were monitored to determine if any alterations correlated with liver pathological changes. gamma-Glutamyltranspeptidase activity in both liver and plasma was markedly increased during initiation by N-2-fluorenylacetamide. Following cessation of carcinogen exposure, gamma-glutamyltranspeptidase remained elevated, providing an indication of past initiation. Administration of phenobarbital after N-2-fluorenylacetamide resulted in an elevation of liver and plasma gamma-glutamyltranspeptidase, but none of the benzodiazepines produced this effect and thus no biochemical evidence of a promoting effect on the liver was observed. Correlations between liver and plasma gamma-glutamyltranspeptidase and the occurrence of foci were excellent, indicating that determination of plasma activity can be used as an index of the process of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed2005

Effect of continuous application of shear stress on liver tissue: continuous application of appropriate shear stress has advantage in protection of liver tissue.

Rapid blood flow changes occur in the liver following a massive resection or in the grafted liver following transplantation, under which shear stress (SS) change induced by the flow change may determine the postoperative results. We observed changes in liver tissue structure and liver-specific function, and consequently assessed SS effect. The cultured liver tissue exposed to continuous application of moderate SS was shown to express and maintain a long-term liver-specific function. There was also evidence showing that destruction of the liver structure was inhibited. However, the cultured liver tissue not exposed to SS or exposed to high SS was shown to lose liver-specific function soon after expression. The liver structure was destroyed in the early stage of incubation. These results suggested that continuous application of appropriate SS has advantages over other types of stresses to protect liver tissue.

Animals↗