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At least 919 records · Page 51Linked to original sources
PubMed2001

Quantification of intrahepatic non-uniform distributions for assessing impaired function of liver using 99Tcm-DTPA-galactosyl serum albumin liver SPECT scintigraphy.

Quantitative evaluation of intrahepatic non-uniform distribution was attempted by functional volumetric analysis of liver single photon emission computed tomography (SPECT) scintigraphy using 99Tcm-diethylenetriaminepentaacetic acid galactosyl serum albumin (99Tcm-GSA) (185 MBq). A total of 148 patients were classified into three groups: diffuse liver disease, liver disease with space-occupying lesions, and non-hepatic disease. The volume obtained at the 10% cut-off threshold from reconstructed liver-specific SPECT images was assumed to be the functional total hepatic volume, and the functional volume rates were calculated every 10% threshold width from 10% to 100%. The hepatic distribution index (D index) was calculated from the sum of absolute differences from the control. The hepatic D index in liver cirrhosis was significantly higher than in hepatitis and other diffuse liver diseases, and the index in liver disease with primary malignant neoplasm was significantly higher than in liver disease with metastasis or a benign-space occupying lesion. Additionally, it was significantly negatively correlated with LHL15, and positively correlated with the clinical severity. However, in stages II and III, with which LHL15 did not significantly correlate, the hepatic D index matched the severity of hepatic impairment. The hepatic D index evaluates distribution of functional hepatocytes and may provide a new clinical method for quantitatively assessing hepatic impairment.

Hepatitis↗
PubMed1982

Alcohol unrelated hepato-biliary disorders in the alcoholic: the role of liver biopsy in determining the aetiology of liver disease.

Alcoholics with abnormal liver function tests are generally assumed to have one of the recognised patterns of alcoholic liver injury. This report described a group of nine patients who were initially thought to have alcoholic liver disease but were found on liver biopsy to have a variety of liver disorders unrelated to alcohol. Liver biopsy showed granulomatous hepatitis in three, primary biliary cirrhosis in two, and cholestasis of unknown cause, large duct biliary obstruction, haemochromatosis with secondary carcinoma and Budd-Chiari syndrome in one each. The histological changes observed in liver biopsy samples are believed to represent a chance occurrence of liver disease due to some agent other than alcohol and illustrates that forms of hepatic disease that affect the population at large can and do occur in heavy alcohol consumers.

Aged↗
PubMed1998

Aggravating action of zymosan on acute liver damage in perfused liver of rats treated with D-galactosamine.

To study the role of Kupffer cells in the aggravation of liver injury, effects of zymosan on acute liver damage were explored using perfused livers of rats 24 h after intraperitoneal injection of D-galactosamine (800 mg/kg). The leakage of lactate dehydrogenase and aspartate aminotransferase into the effluent was used to indicate acute liver damage. Infusion of zymosan (30 microgram/ml) into the portal vein rapidly increased the leakage of lactate dehydrogenase and aspartate aminotransferase from galactosamine-treated liver with decreased perfusion flow. Pretreatment of animals with gadolinium, which diminished an immunostaining of resident macrophages in the injured liver, significantly attenuated the flow reduction induced by zymosan, whereas it did not affect the increases in enzyme leakage. Infusions of PGF2alpha, PGE2, and leukotriene D4, the eicosanoids mainly produced by Kupffer cells, decreased perfusion flow without rapid augmentation of enzyme leakage from galactosamine-treated liver. These results indicate that zymosan potentiates acute liver damage after galactosamine injection and suggest that certain types of nonparenchymal cells other than Kupffer cells are mainly involved in the action of zymosan.

Acute Disease↗
PubMed1998

[Detection of HGV NS5 antigen in liver tissue of patients with chronic liver disease].

OBJECTIVE: To investigate the existence of hepatitis G virus (HGV) in liver tissue. METHODS: HGV NS5 antigen was detected by immunohistochemical method in paraffin-embeded liver tissue of autopsy patients with chronic liver disease. RESULTS: Among 110 samples, 32.7% (36/110) had been detected out HGAg in their liver. When serologica marker was used, the detection rate was 21% (4/19) in HNA-E, 36% (25/69) in HBV and 32% (7/22) in HCV infectious group, respectively. HGAg expression in hepatocytes was also found pathologically in 22% of 45 patients with active cirrhosis, 43% of 47 patients with hepatocellular carcinoma, and 33% of 18 patients with chronic fulminent hepatitis. The staining signal of HGV NS5 antigen was mainly located in the cytoplasm of liver or neoplasm cells, and the positive cells were distributed diffusely in pseudolobule or liver tissues. CONCLUSION: The infection of viral G is often seen in liver tissue of patients with chronic liver disease.

Adult↗
PubMed2001

Development of liver size and perfusion after reduced-size liver transplantation in children.

The technique of segmental liver transplantation (s-LTx) provides a method to overcome the shortage of suitable livers for small recipients. Patient survival rates are parallel to those obtained with whole liver transplantation (w-LTx). For long-term rehabilitation, adaptive liver growth and adequate perfusion is crucial; however, morphometric and hemodynamic parameters in growing children with s-LTx are not available. Seventeen children who received a s-LTx and 25 with a w-LTx who had follow-up evaluation 1 and 2 yr after LTx were studied. Mean age at time of transplantation was 4.3 +/- 3.5 yr for s-LTx and 10.3 +/- 6.0 yr for w-LTx, mean height 98 +/- 21 cm and 122 +/- 30 cm respectively. At follow-up evaluation mean values for liver enzymes, bilirubin and prothrombin time were in the normal ranges for both groups. Liver dimensions were measured by gray scale ultrasound, and hemodynamic parameters by Doppler sonography in the portal vein and hepatic artery using an Acuson 128 machine. Maximal (Vmax), minimal (Vmin) and time-average velocity (TAV) were measured and the resistive index (RI) calculated. We found that 1 and 2 yr after LTx liver dimensions were at a mean in the upper normal range of healthy controls. Spleen size was above the normal range and did not show any tendency towards regression. Mean Vmax in the hepatic artery in s-LTx and w-LTx was 48 cm/sec vs. 28 cm/sec after 1 yr and 30 cm/sec vs. 35 cm/sec after 2 yr, the RI 0.66 vs. 0.55 and 0.59 vs. 0.73, respectively (p for all parameters > 0.05). Maximal portal vein flow was 25 cm/sec in s-LTx vs. 29 cm/sec in w-LTx. Blood flow calculated by vessel diameter and TAV showed no statistical difference between both groups. In conclusion, liver size after s-LTx and w-LTx was increased to the upper normal range, and portal vein blood flow velocities were within the normal range. Vmax in the hepatic artery was reduced in s-LTx; however, the reduction was to the same extent as in w-LTx. In the view of long-term functional adaptation, s-LTx is not inferior to w-LTx.

Adolescent↗
PubMed1984

[Experimental and clinical studies on regeneration of the cirrhotic liver after major hepatectomy: comparison with the volume and function of the normal liver during recovery].

Experimental and clinical studies on the role of liver cirrhosis in the impaired hepatic regeneration after major hepatectomy were done comparing the changes of liver function measured by indocyanine green tolerance and hepaplastin test. In experimental cirrhosis induced by dimethylnitrosamine administration, canine livers revealed that the recovery of volume after 70% hepatectomy was slow but efficient in survivors. Two patients who had hepatic lobectomy with normal remaining liver showed complete recovery in both volume and function, but 2 patients with remaining liver of non-cirrhotic fibrosis showed slow recovery of liver function. Two cirrhotic survivors after lobectomy and segmentectomy revealed very slow recovery in function but gained sufficient volume. The study indicated that increased efficiency of liver function in the early stage of regeneration supported by effective hepatic blood flow was essential for the successive recovery of hepatic volume and for the survival in liver cirrhosis.

Adult↗
PubMedDate not supplied

[Role of the liver in the regulation of glucose metabolism in diabetes and chronic liver disease].

The liver plays a major role in the regulation of glucose metabolism: plasma glucose concentration is the result of peripheral glucose utilization and liver production. Several hormones, including insulin, glucagon, growth hormone, cortisol, and catecholamines contribute to the regulation of glucose metabolism by the liver. In this review, we examine hepatic glucose metabolism, in particular the actions of insulin and contrainsular hormones on glucose hepatic uptake and production in patients with diabetes or chronic liver disease. The most frequent patterns of hepatic involvement that take place during diabetes, i.e. nuclear glycogenesis, steatosis, portal fibrosis, and diabetic steatonecrosis, are discussed. Also considered are anomalies of glucose homeostasis observed in chronic liver disease, including glucose intolerance, diabetes, and hypoglycemias. There is a strong correlation between diabetes mellitus and the liver: diabetic patients have typical histological lesions, while several glucose metabolism alterations are commonly found in subjects with chronic liver disease. The pathogenesis of impaired glucose metabolism during chronic liver disease has not yet been fully understood: further clinical and experimental studies should clarify this issue.

Chronic Disease↗
PubMedDate not supplied

Orthotopic liver transplantation in 4 patients with portal hypertension and non-cirrhotic nodular liver.

BACKGROUND/AIMS: Non-cirrhotic nodular liver may occasionally be associated with portal hypertension, with complications such as ascites, bleeding esophageal varices and sometimes hepatic encephalopathy. Four patients treated with transplantation are hereby described. METHODOLOGY: All 4 patients had orthotopic transplantation. Cyclosporine based immunosuppression was used in all patients. RESULTS: The first patient had nodular regenerative hyperplasia in the resected native liver and in the graft seven years after the transplant, what could be considered as recurrence of the disease. There were two more cases of nodular regenerative hyperplasia; one of them was diagnosed 9 years before transplantation, but he developed progressive liver failure. The fourth patient had chronic renal failure and a nodular liver. His general condition and fear of untreatable ascites after a portosystemic shunt, prompted us to perform a liver-kidney transplantation. CONCLUSIONS: Portal hypertension associated with non-cirrhotic nodular liver disease can be, in general, successfully treated with medical and endoscopic measures, or in certain more serious cases with portosystemic shunting. Nevertheless, there are certain cases where liver insufficiency, associated diseases or the unawareness of the pathological diagnosis determines a liver transplantation.

Adult↗
PubMed1997

Comparison of effect of tumor promoter treatments on DNA methylation status and gene expression in B6C3F1 and C57BL/6 mouse liver and in B6C3F1 mouse liver tumors.

The effects of different liver tumor-promoting treatments (i.e., a choline-devoid, methionine-deficient (CMD) diet, phenobarbital (PB), or both) on Ha-ras and raf methylation status and expression were determined in mouse strains with different susceptibilities to liver tumor formation: the relatively sensitive B6C3F1 and the relatively resistant C57BL/6. Additionally, B6C3F1 mouse liver tumors, spontaneous or PB induced, were assessed for alterations in global DNA methylation status and expression of Ha-ras and raf. The CMD diet led to hypomethylation of Ha-ras and raf after 12 wk of administration in B6C3F1 and C57BL/6 mice. At this early phase of tumor promotion, the frequency of increased expression of both Ha-ras and raf mRNAs was higher in the B6C3F1 but not the C57BL/6 mice. This is a mechanism that may, in part, underlie the heightened sensitivity of the B6C3F1 mouse to liver tumorigenesis. Subpopulations of B6C3F1 mouse liver tumors displayed altered global methylation status, with both hypomethylation and hypermethylation evident. Carcinomas were significantly more hypomethylated than adenomas. The level of raf mRNA was not changed in spontaneous or PB-induced B6C3F1 mouse liver tumors. Increased expression of Ha-ras was evident in some spontaneous B6C3F1 liver tumors and in most of the PB-induced liver tumors. These experiments support the concept that altered DNA methylation plays a key role in tumorigenesis and indicate that the high propensity of the B6C3F1 mice to liver tumorigenesis may be due, in part, to a decreased ability to maintain normal methylation status.

Animals↗
PubMed2001

Expression of alpha-amylase gene in rat liver: liver-specific amylase has a high affinity to glycogen.

The reactivity of rat liver alpha-amylases with maltotriose (G3), maltopentose (G5) and glycogen has been investigated. Liver amylases were found to be glycosylated and to have a molecular mass of 50 kDa by Western blotting using an anti-human salivary amylase antibody. The glycosylated liver amylases were found to be capable of G3- and G5-hydrolysis and of glucose formation, as demonstrated by thin-layer chromatography. When the amylase preparation was exposed to different concentrations of glycogen and run on a cellulose acetate membrane, the mobilities of rat liver amylases significantly decreased with tailing directly from the point of origin. In contrast, rat salivary amylases were not so much. These results indicate that rat liver amylases have a strong affinity to glycogen. We confirmed the expression of liver-specific amylases in rat liver by reverse transcriptional-polymerase chain reaction (RT-PCR); PCR products showed one band of an expected size of 474 bp using primers tested in the present study. A partial nucleotide sequence was then determined. When compared with the gene of mouse liver amylase, the substitution of 26 bases out of 434 bases was elucidated. The present data demonstrate the presence of liver-specific amylases in rats.

Animals↗
PubMed1996

Repeated liver resection for recurrent liver cancer.

Patients with cancer recurrence limited to the liver alone after a first liver resection may be candidates for a repeat resection. Some 191 second and ten third liver resections for recurrent colorectal metastases, and 128 second and ten third liver resections for recurrent hepatocellular carcinoma (HCC), were evaluated after reviewing the literature. The 5-year survival rate after second liver resection for colorectal metastases was 26 per cent with a median survival time of 30 months. Mortality and morbidity rates were 1.2 and 27.4 per cent respectively. The 5-year survival rate after second resection for HCC was 40 per cent with a median survival time of 40 months. The operative mortality rate was 2.3 per cent; morbidity occurred in 13 per cent of patients with HCC. Survival after primary colorectal resection was significantly better for patients with metachronous metastases than for those with synchronous disease; survival correlated with a long interval between the first and second liver resection (in both colorectal liver cancer and HCC). Repeated liver resection may be performed in selected patients and yield a similar survival to that obtained after first liver resection.

Adult↗
PubMed1995

The antifreeze protein genes of the winter flounder, Pleuronectus americanus, are differentially regulated in liver and non-liver tissues.

The synthesis of winter flounder (Pleuronectus americanus) antifreeze protein (AFP) mRNAs in the liver is seasonally regulated by the pituitary gland. With the recent discovery that AFP mRNAs are also present in several non-liver tissues, the aim of the present investigation was to compare the regulatory mechanisms of AFP genes in liver and non-liver tissues. Northern blot analyses indicate that the level of liver AFP mRNA undergoes a several hundred fold difference between the winter and summer months, while AFP mRNAs from gills and kidneys exhibit only a modest 5-10 fold seasonal variation. As expected, the liver AFP mRNA in the hypophysectomized fish was increased by over 40 fold. However, no significant increase was observed for the non-liver AFP mRNAs upon hypophysectomy. These investigations suggest that AFP mRNAs in liver and non-liver tissues are differentially regulated.

Animals↗
PubMed1995

Distinct patterns of cyclin D1 regulation in models of liver regeneration and human liver.

The expression of cyclin D1 and associated cdks was examined in models of liver regeneration and human liver specimens. In mouse liver after 70% partial hepatectomy, there was > 20-fold induction of cyclin D1 mRNA and protein, beginning prior to peak DNA synthesis. In normal rat liver, basal levels of cyclin D1 protein were significantly higher than in the mouse. After hepatectomy in the rat, cyclin D1 mRNA was induced 6- to 10-fold, while the protein levels changed < 2-fold and did not parallel changes in the mRNA. Cyclin D1 protein was detected in freshly isolated rat hepatocytes, but this diminished within 6 hours in culture. After growth stimulation with HGF, cyclin D1 mRNA was induced 3- to 5-fold and its protein > 20-fold in rat hepatocytes. Immunoprecipitation of cyclin D1 demonstrated its association with cdk4 but not cdk5 in regenerating liver. In human liver biopsy specimens, cyclin D1 protein was detectable in normal liver and induced 2- to 10-fold in mitotically active liver following transplantation. These results suggest that the regulation of cyclin D1 protein in human liver may more closely parallel the mouse than the rat hepatectomy model. Furthermore, cyclin expression in primary cells in culture may differ significantly from that observed in vivo.

Animals↗
PubMed1999

Change of liver function in hypertrophying lobe of rabbit liver after portal branch ligation.

Preoperative portal embolization (PE) is useful for the prevention of postoperative liver failure after extended hepatectomy. However, clinical evaluation of liver function in the hypertrophying lobe after PE has not been studied. Here we report functional changes in the hypertrophying lobe using a 80% portal-branch-ligation rabbit model. Liver function was evaluated by the expression of liver-specific genes detected by Northern blot analysis and plasma disappearance rate of indocyanine green (ICG). The weight of the unligated lobe after portal ligation increased about twofold on the 7th postoperative day (POD) and about threefold on the 14th POD. The mRNA levels of the liver-specific genes (albumin, aldolase B, and tyrosine aminotransferase) in the unligated lobe decreased to about 50% on the 1st POD and returned to the preoperative levels on the 7-14th POD. In contrast, the expression of histone H2B mRNA increased on the 3rd-7th POD. The plasma disappearance rate of ICG (K-ICG) in the rabbit that has only the unligated lobe did not significantly change during the first 7 days, but then improved and recovered to 80% of that in the rabbit that has whole liver on the 14th POD. These results indicate that liver function of the hypertrophying lobe after portal branch ligation does not increase during the first 7 days despite an increase in liver weight. This finding suggests that the compensatory hypertrophying liver is enlarging without functional augmentation in the early period after PE.

Animals↗
PubMed1989

Morphological, physiological and biochemical alterations in livers of rodents induced by protease inhibitors: a comparison with old livers.

A "Protease inhibitor model of aging" has been proposed primarily based on observations on brain tissues exposed to a thiol protease inhibitor, leupeptin (Ivy et al., 1984a). In order to validate this model in terms of a mechanism of cellular aging, as well as of lipofuscin formation in particular, attempts have been made to induce lipofuscin in hepatocytes in young rodent (rat and mouse) livers by continuous i.p. infusion of two different thiol protease inhibitors, leupeptin and E-64C. With doses of leupeptin higher than 1.0 mg/100g/day for 2 wks, a fine granular lipofuscin-like deposition with distinct yellowish-green fluorescence was induced in young rat hepatocytes. The deposition became greater in degree with increasing leupeptin doses. In Kupffer cells and other endothelial cells, fluorescent granules were also induced. In contrast to rat livers, lipofuscin-like pigments induced in hepatocytes in mice were much less, even with a higher dose (20 mg/100 g/day). E-64C also induced the accumulation of lipofuscin-like pigments at a dose of 5 mg/100 g/day, their characteristics being very similar to those induced by leupeptin, but the accumulation being smaller in degree. The fluorescence of leupeptin induced lipopigments was yellowish-green having a peak around 520 nm in emission profile, closely resembling that observed in old rat livers. The hepatobiliary transport functions such as biliary transport maximum (Tm) for sulfobromophthalain and the biliary recovery of iv injected ouabain which are known to decline with age tended to decline in young (6-wk-old) rats administered with leupeptin at a dose of 5 mg/100 g/day for 2 wks. On the other hand, dolichol concentration in leupeptin treated livers was not increased in comparison to control livers, whereas in old rat livers, the dolichol concentration was more than 2 times greater than in young livers. A clear-dose-dependent deposition of ceroid-lipofuscin induced in young rodent livers by protease inhibitors strongly suggests that the "Protease inhibitor model" is generally valid not only for the brain but for other tissues such as the liver, and for two different thiol protease inhibitors.

Aging↗
PubMed1992

Studies on the participation of different T cell subsets in rat liver allograft rejection. Comparison of liver with heart graft.

In this study, we investigated which subsets of rat T cells (CD8+ vs. CD4+) are involved in the rejection of liver allografts by the in vivo administration of monoclonal antibody (OX-8 or OX-38, and W3/25 MAb) into thymectomized recipient Lewis (RTI(l)) rats prior to DA (RTI(a)) liver transplantation. We also compared the results of allograft survival of liver and heart transplants under the same experimental conditions. In order to deplete either CD8+ T cells or CD4+ T cells from recipient animals, 0.4 ml of OX-8 (ascitic form) or a 0.8 ml cocktail of MAb W3/25 and OX-38 (0.4 ml each) was injected into thymectomized recipient rats, respectively. Untreated Lewis rats consistently rejected donor DA liver grafts between 9 and 11 days (n = 7, 9.8 days +/- 1.1 days). In contrast, anti-CD8 MAb pretreatment extended the survival times of DA liver grafts for up to 40 days (n = 5, 26.8 days +/- 8.4 days). Furthermore, survival of DA liver grafts was significantly prolonged in Lewis rats that had been pretreated with anti-CD4 MAb (n = 7, 35.6 days +/- 17.9 days). Two out of seven recipient animals survived for more than 60 days. For heart transplantation, untreated Lewis rats rejected DA heart grafts between 6 and 8 days after operation (n = 6, 6.5 days +/- 1.2 days). Anti-CD4 MAb treatment prolonged heart graft survival for more than 60 days in all cases (n = 3, > 60 days). However, there was virtually no effect of anti-CD8 MAb treatment on heart graft survival (n = 4, 7.0 days +/- 0.9 days). These results suggested that when whole MHC disparity prevailed between donor and recipient, both subsets of T cells were required for the rejection of liver allografts and that class II reactive T cells predominantly mediated liver graft rejection. Furthermore, CD8+ T cells played a differential role in the rejection of rat liver and heart allograft.

Animals↗
PubMed1998

Implications of heat shock proteins during liver surgery and liver perfusion.

Cells primed by sublethal stress transiently overproduce heat shock proteins (HSPs) and thereby develop tolerance to the next lethal stress. This response in organisms is called the stress response and involves the induction of HSPs. To assist the liver in developing tolerance for warm ischemia-reperfusion injury, which sometimes jeopardizes the patients after extended surgery for malignancies with vascular invasion in the liver, basic experiments to activate the stress response using stress preconditioning were performed. Heat shock preconditioning in rat livers has been shown to induce tolerance against warm ischemia-reperfusion injury in normal, fibrotic, and steatotic livers. Ischemic preconditioning using short-term Pringle's maneuver and pharmacological preconditioning using doxorubicin were also effective. In rats, heat shock preconditioning protected livers from free radical injury induced by the oral administration of carbon tetrachloride. The above data were supported by animal survival, suppression of serum transaminase levels, and improved energy status of the liver after intervention. Increased production of HSP72 was observed after preconditioning. In addition, the significance of HSP production as a stress parameter was demonstrated during the reperfusion of congested portal blood to the ischemic liver. The ill effect of congested portal blood could not be detected by conventional parameters but was detected by observing the increase in HSP72 production. Stress preconditioning seems to be a promising strategy to counter the damaging effect of hepatic warm ischemia during liver surgery and liver perfusion.

Animals↗
PubMed1987

Extracorporeal isolated pig liver perfusion: influence of various blood primes on liver function.

Extracorporeal isolated pig liver perfusion was performed in three groups of five piglets each to assess the influence of different blood primes on liver function. All prime volumes were hemodiluted to a hematocrit of 0.3-0.35 and adjusted to a pH of 7.35-7.45 with sodium bicarbonate at a temperature of 38 degrees C. Fresh slaughterhouse blood was collected, mechanically filtered and used in Group A, whereas analogously collected blood was biologically filtered by passage through the organism of the piglet in Group B. In Group C, the priming blood consisted of autologous blood gained during hepatectomy by a special technique. A high potassium concentration (10.4 +/- 0.94 mmol/l) in Group A and impurities of the slaughterhouse blood in both Groups A and B led to rapid edema formation and an increase in vascular resistance of the perfused liver, and a prolonged perfusion was not achieved. In the third group, however, liver perfusion over a period of 5 h without any deterioration of liver function was possible. Beside liver function tests, oxygen consumption, the macroscopic aspect and bile flow of the liver seemed to be the most reliable parameters in assessing the function of the isolated perfused pig liver. Our technique to gain autologous blood can be recommended not only for extracorporeal liver perfusion but also for any other extracorporeal isolated organ perfusion.

Animals↗