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At least 451 records · Page 25Linked to original sources
PubMed2003

[The effects of L-arginine and NG-nitro-L-arginine methylester on lipopolysaccharide and lipoteichoic acid induced liver injury in the rat].

BACKGROUND: Whether nitric oxide (NO) protects or impairs the liver function and structure during the early phase of sepsis is still controversial. The aim of this study is to evaluate the effect of NO on lipopolysaccharide (LPS) or lipoteichoic acid (LTA) induced liver injury in rats. METHODS: One hundred twenty-six Wistar rats were assigned randomly and equally to LTA and LPS groups. Each group was divided into three subgroups which received saline, L-Arginine (L-Arg) or NG-nitro-L-arginine methylester (L-NAME) consecutively, one hour prior to either 5 mg/kg LPS or 3 mg/kg LTA injection. Plasma nitrite plus nitrate [NOx] were measured. Liver injury was assessed by measuring the rises in circulating liver enzymes and by scoring the extent of liver necrosis. RESULTS: Administration of L-NAME+LPS not only reduced [NOx] production but also enhanced liver damage. LNAME+ LTA caused an increase in the plasma levels of [NOx] (p=0.0006), and produced sinusoidal enlargement in liver. L-Arg protected the hepatocytes against LPS injury, whereas, enhanced the liver damage in the LTA group. CONCLUSION: Our data indicated that overproduction of NO exerts detrimental effect on LTA-treated rats while providing a protective function in LPS group.

Animals↗
PubMed1979

Rapid increase of fibrinolytic activity in pig and rat after exclusion of the liver from the circulation and its control by various organs.

Liver-bypass in the pig and the rat instantly results in a marked increase of fibrinolytic activity. Within 1--2 hours this increase is followed in rats by a normalization. A new increase can be obtained by intravenous Carbachol injection. Removal of organs results to various degrees -- most pronounced after bilateral nephrectomy -- in reduction of control value of fibrinolytic activity before liver-bypass. In rats with adrenalectomy plus splenectomy there is no normalization of liver-bypass-induced increased fibrinolytic activity.

Adrenalectomy↗
PubMed2006

Morphological and histochemical analyses of living mouse livers by new 'cryobiopsy' technique.

A new 'cryobiopsy' (CB) technique has been invented for freezing the functioning livers of living mice in vivo without stopping their blood circulation. Livers of anesthetized mice were pinched off with pre-cooled CB forceps and immediately plunged into isopentane-propane cryogen. They were routinely freeze-substituted in acetone containing paraformaldehyde for light microscopy (LM) or osmium tetroxide for scanning electron microscopy (SEM). By freeze-fracturing some of them with a scalpel in liquid nitrogen before the freeze-substitution, well-preserved tissue areas were exposed only for SEM. They were either embedded in paraffin wax for LM or infiltrated with t-butyl alcohol followed by freeze-drying for SEM. Serial paraffin sections were stained with hematoxylin-eosin (HE) or histochemical periodic acid-Schiff (PAS) reaction. By HE-staining, the tissue surface areas were often compressed with the CB forceps and sinusoidal erythrocytes became aggregated side by side. In slightly deeper tissue areas, however, hepatic sinusoids were widely open with flowing erythrocytes. Lots of PAS-reaction products were well preserved in hepatocytes of the CB specimens. On the contrary, they were unevenly distributed in hepatocytes of conventionally quick-frozen specimens, and often lost in those of the conventionally dehydrated specimens. By SEM, some cell organelles, such as mitochondria and endoplasmic reticulum, and also dilated fenestrae of endothelial cells, open Disse's spaces and bile canaliculi appeared to be under normal blood circulation in the prepared CB samples. The new CB technique would be easy and useful for repeated examination of functioning organs of a living animal.

Animals↗
PubMed1983

Liver membrane antibodies in alcoholic liver disease. II. Antibodies to ethanol-altered hepatocytes.

Using an indirect immunofluorescence technique, circulating liver membrane antibodies against normal rabbit hepatocytes and ethanol-altered rabbit hepatocytes have been sought in a series of patients with histologically confirmed alcoholic liver disease. Liver membrane antibodies against normal hepatocytes were found in 18 (28%) of the 65 sera examined, but with ethanol-altered hepatocytes as substrate liver membrane antibodies were found in 48 (74%) of the sera. Isolation of F(ab')2 fragments confirmed that the positive results were due to antibody binding. Liver membrane antibodies against ethanol-altered hepatocytes are peculiar to alcoholic liver disease, and there is a similar incidence in the various histological types of alcoholic liver disease. Absorption studies suggest that the liver membrane antibodies are directed against new or altered antigens which are not present in normal hepatocytes. These new or altered antigens may also appear after pretreatment with other primary alcohols and seem likely to be induced by a haptenic effect of the alcohol or a metabolic break-down product. These studies represent a novel approach to the further investigation of the possible role of immunological mechanisms in alcohol-induced liver injury.

Absorption↗
PubMed1992

Involvement of nonparenchymal cells in oxygen-dependent hepatic injury by allyl alcohol.

Allyl alcohol injury to hepatocytes in the perfused liver is oxygen-dependent. It is not known if this injury involves direct action of allyl alcohol on hepatocytes or requires participation of other cell types (e.g., Kupffer cells) present in the liver. Accordingly, the action of allyl alcohol (100-500 microM) on isolated hepatocytes was studied using cells maintained at either 95 or 21% O2. Allyl alcohol toxicity, as indexed by trypan blue uptake, lactate dehydrogenase release, and ATP content, did not differ in the two groups of cells, suggesting that O2 dependency of allyl alcohol toxicity involves other cell types. Administration of allyl alcohol (30 or 40 mg/kg, ip) to rats caused extensive hepatic necrosis localized primarily to periportal regions. To test the involvement of Kupffer cells in the genesis of this injury, male rats (200-350 g) were treated with gadolinium chloride (GdCl3, 10 mg/kg, iv) which diminishes Kupffer cell function and number. The extent of hepatic damage assessed by light microscopy and serum enzymes, aspartate aminotransferase and alanine aminotransferase, was markedly attenuated by pretreatment of rats with GdCl3 24 hr prior to allyl alcohol injection. Thus, O2-dependent hepatic necrosis caused by allyl alcohol involves the presence of Kupffer cells. Since GdCl3 did not prevent toxicity in the perfused liver, circulating blood elements may also contribute to injury of the liver by allyl alcohol in vivo.

1-Propanol↗
PubMed1992

[Experimental heterotopic transplantation of the liver with anastomosis of the portal vein to the distal end of the splenic vein].

A model of heterotopic liver transplantation had been studied. The graft was laid under the recipient liver and the portal blood flow was supplied by anastomosis with the distal part of the splenic vein. Both liver can then receive portal blood through two parallel portal circulation. Liver function of transplant was satisfactory at three months after transplantation. Their had been no alteration of the recipient liver during the same period.

Anastomosis, Surgical↗
PubMed1994

[Heterotopic experimental liver transplantation with portal revascularization of the graft on the distal splenic vein of the recipient].

A model of heterotopic liver transplantation had been studied. The graft was laid under the recipient liver and the portal blood flow was supplied by anastomosis with the distal part of the splenic vein. Both liver can then receive portal blood through two parallel portal circulation. Liver function of transplant was satisfactory at three months after transplantation. Their had been no alteration of the recipient liver during the same period.

Anastomosis, Surgical↗
PubMed2003

Suppressed complement activation in human decay accelerating factor transgenic porcine liver cross-circulated with nonhuman primates.

BACKGROUND: We developed an extracorporeal liver perfusion (ECLP) system as a liver-assist device. In this study, we evaluated the safety of the ECLP using human decay accelerating factor (hDAF) transgenic porcine livers in healthy baboons. METHODS: Livers were isolated from five hDAF transgenic pigs and five nontransgenic pigs for the ECLP. Ten cross-circulations between the ECLP and healthy baboons were performed without immunosuppressive agents. Cross-circulation was discontinued in any of the following circumstances: elevated hepatic arterial (>200 mm Hg) or portal (>60 mm Hg) perfusion pressure, massive exudate from the graft liver, mild macroscopic hemolysis, thrombocytopenia, or 24-hr well-conditioned cross-circulation. RESULTS: The cross-circulations with nontransgenic porcine livers were discontinued at 4.4+/-1.2 hr (mean+/-standard deviation) because of high perfusion pressure (n=2) or hemolysis (n=3). Three cross-circulations with hDAF transgenic porcine livers were performed for 24 hr; the other two cross-circulations were discontinued at 13 and 17 hr because of massive exudate and thrombocytopenia, respectively. The duration was 20.4+/-5.1 hr. Deposition of membrane attack complex in the hDAF transgenic porcine liver was less than that in the nontransgenic liver, although immunoglobulin-M deposition was comparable. The porcine livers showed no apparent interlobular bleeding or lobular necrosis. All porcine livers maintained bile production during the cross-circulation. No baboons showed any serious complications after the cross-circulation. CONCLUSION: The hDAF transgenic porcine liver reduced complement activation in xenoperfusion with healthy nonhuman primate blood and led to extended duration of cross-circulation.

Animals↗
PubMedDate not supplied

The afferent circulation of the liver in patients with primary hepatocellular carcinoma.

BACKGROUND/AIMS: The data on the afferent circulation of the liver, in patients with primary hepatocellular carcinoma, are controversial or non-existent. MATERIALS AND METHODS: The authors measured hepatic arterial and portal venous flow intra-operatively by transit time ultrasonic volume flowmetry. RESULTS: In patients with primary hepatocellular carcinoma, the hepatic artery flow increased to 0.55 +/- 0.21 l, as compared with the control value of 0.37 +/- 102 l/min (p < 0.01). The portal venous flow decreased from 0.61 +/- 0.212 l/min to 0.47 +/- 0.203 l/min p < 0.01). Owing to the opposite changes in the afferent circulation, the total hepatic blood flow did not change significantly. The ratio of hepatic arterial flow to portal vein flow increased to 1.239 +/- 0.246 in patients with hepatocellular carcinoma, which is twice the basic control value (0.66 +/- 0.259 l/min). After resection, this ratio showed virtually no change. The surgical intervention, that is resection of the liver, did not significantly alter hepatic artery and portal venous flow, although total hepatic blood flow decreased significantly (p < 0.01). The pronounced increase in the ratio of hepatic arterial flow may be attributed to the decrease in portal venous flow caused by the primary hepatocellular carcinoma. The decrease in venous flow can most probably be explained by compression and infiltration of the intrahepatic branches of the portal vein. As we pointed out, the decrease in portal venous circulation leads to an increase in hepatic arterial flow. CONCLUSIONS: On the basis of our initial results, it seems probable that the ratio of the two circulations represents a diagnostic tool for the altered circulation in patients with hepatocellular carcinoma. The significance of this phenomena is not yet quite clear, but a review of the literature shows that similar observations have not been reported. In practical terms this phenomenon may be useful from the point of view of US and Doppler US diagnosis, e.g. in the case of a hypo-echoic or hyperechoir, mass in the liver, increased blood flow in the hepatic, artery, and decreased portal venous flow, a malignant liver tumor is virtually certain. The authors hypothesise that any pathology in the liver may lead to a primary decrease in PVF and a subsequent increase in HAF.

Adult↗
PubMed2001

Plasma concentration of tissue inhibitor of matrix metalloproteinase 1 in patients with colorectal carcinoma.

BACKGROUND: The expression of tissue inhibitor of matrix metalloproteinase (TIMP) 1 in tumour tissue from patients with colorectal carcinoma has been reported to be related to disease progression. However, the clinical significance of plasma TIMP-1 has not been fully elucidated. METHODS: The plasma level of TIMP-1 protein was determined by enzyme-linked immunosorbent assay in samples from 54 patients who underwent resection of the primary tumour. RESULTS: Plasma TIMP-1 levels were associated significantly with depth of invasion and metastasis to lymph nodes and liver. Circulating TIMP-1 levels were significantly higher in patients with serosal invasion, liver metastases and Dukes' stage C tumours. Using a cut-off value of 160 ng/ml, serosal invasion and Dukes' C stage could be predicted with an accuracy of 68.5 per cent. With a cut-off value of 170 ng/ml, metastasis to the lymph node and liver could be predicted with an accuracy of 66.7 and 70.4 per cent respectively. These values were greater than those for carcinoembryonic antigen and CA19-9. CONCLUSION: These data suggest that the plasma concentration of TIMP-1 correlates with both invasion and metastasis in patients with colorectal carcinoma.

Adult↗
PubMed1998

Central role of the adipocyte in insulin resistance.

Mechanisms of insulin resistance in subjects at risk for type 2 diabetes remain to be elucidated. Insulin acts slowly in vivo, but rapidly in vitro, suggesting that the pathway insulin traverses from B-cell to insulin sensitive tissue may be altered in diabetes. An important component of that pathway is transport of insulin across the capillary endothelium. Several groups have demonstrated that insulin resistance may result from reduced capillary permeability to insulin--it remains to be determined whether reduced permeability contributes to insulin resistance in any stage leading to type 2 diabetes. Interestingly, the transport of insulin across the endothelial barrier not only limits the rate of insulin to stimulate glucose uptake by skeletal muscle, but appears also to determine the rate at which insulin suppresses liver glucose output. Because the liver circulation is fenestrated, it is not possible that insulin transport into the liver is the rate determining step for suppression of liver glucose output. An alternative hypothesis was considered--that insulin is transported into an extrahepatic tissue. A "second signal" is generated by the extrahepatic tissue, the signal is released into the blood, and the signal in turn controls hepatic glucose output. Several lines of evidence suggest that the second signal is free fatty acids (FFA): 1) There is a strong correlation between FFA and liver glucose output under a variety of experimental conditions. 2) If FFA are maintained at basal concentrations during insulin administration, glucose output fails to decline. 3) If FFA are reduced independent of insulin administration, glucose output is reduced. These three points support the concept that insulin, by regulating adipocyte lipolysis, controls liver glucose production. Thus, the adipocyte is a critical mediator between insulin and liver glucose output. Evidence that FFA also suppress skeletal muscle glucose uptake and insulin secretion from the B-cell supports the overall central role of the adipocyte in the regulation of glycemia. Insulin resistance at the fat cell may be an important component of the overall regulation of glycemia because of the relationships between FFA and glucose production, glucose uptake, and insulin release. It is possible that insulin resistance at the adipocyte itself can be a major cause of the dysregulation of carbohydrate metabolism in the prediabetic state.

Adipocytes↗
PubMed2000

[Treatment of non-resectable liver tumors with percutaneous interstitial laser coagulation while interrupting blood circulation to the liver].

OBJECTIVE: To evaluate, in patients with hepatocellular carcinoma or colorectal carcinoma disseminated to the liver, treatment with interstitial laser coagulation (ILC) during temporary occlusion of vascular inflow in the liver: feasibility, complications and initial tumour response. DESIGN: Prospective, descriptive. METHODS: Patients were included if their tumours were surgically irresectable and smaller than 4 cm in diameter and did not exceed a number of 3. ILC was performed under general anaesthesia, basically via a percutaneous approach. Vascular inflow was occluded during laser treatment. Twenty-four hours after ILC a triphasic spiral CT was performed to assess the result of the treatment. RESULTS: In 10 patients 14 hepatic tumours were lasered in 12 treatment sessions (10 percutaneous and 2 at laparotomy). After 5 treatment sessions, complications were observed of which pain at the insertion site of the catheters was the most frequent. For 6 out of the 10 patients with percutaneous procedures, discharge was within 24 hours after ILC. Nine out of the 14 tumours (65%) were completely coagulated. CONCLUSION: ILC with vascular inflow occlusion is a safe and feasible technique that can be performed during a short hospital stay. Initial tumour response is 65% and these results justify determination of duration of response in a larger group of patients.

Aged↗
PubMed1988

Liver autoreactivity in acute virus A, B and non-A, non-B hepatitis.

As part of an investigation into the question of whether virus-induced autoreactivity might contribute to liver damage in viral hepatitis, serial studies (from onset through recovery) of circulating liver autoantibodies have been performed in patients with uncomplicated acute virus A (AVH-A), B (AVH-B) and non-A, non-B (AVH-NANB) hepatitis in whom the time of onset of symptoms could be precisely documented. One hundred and forty-four sera from 35 patients were tested by radioimmunoassay for autoantibodies against the liver-derived lipoprotein complex, LSP, and also against one of its constituents--the asialoglycoprotein receptor, known as hepatic lectin (HL). Anti-LSP antibodies were found in all 10 patients with AVH-A, in 17/18 with AVH-B and in 3/7 with AVH-NANB at titres that declined during recovery. Anti-HL antibodies were detected concurrently in 6 of the AVH-A patients and in 5 with AVH-B but on only 1 occasion in 1 patient with AVH-NANB. Transient cellular immunity to LSP, assayed by a T-lymphocyte migration inhibitory factor test, was detected in 4 of the 6 AVH-B patients tested, 2 of whom also showed concurrent reactivity to HL, but these cellular immune responses did not correlate with production of anti-LSP and/or anti-HL. The findings indicate that humoral immune responses to liver cell surface antigens are frequently triggered by hepatitis A and B viruses, possibly via induction of autoreactive, T-cell independent, liver antigen-specific B lymphocytes. These liver-specific autoreactions have the potential to contribute to hepatocellular damage in virus A and B hepatitis but it seems unlikely that autoimmunity plays a significant pathogenetic role in NANB viral infections.

Adult↗
PubMed1999

Detection of aberrant p16 methylation in the plasma and serum of liver cancer patients.

We have studied the feasibility of detecting tumor-associated aberrant p16 methylation in the circulation of patients with hepatocellular carcinoma (HCC). We extracted DNA from the tumor tissues and peripheral blood plasma or serum of 22 HCC patients. p16 methylation was found in 73% (16 of 22) of HCC tissues using methylation-specific PCR. Among the 16 cases with aberrant methylation in the tumor tissues, similar changes were also detected in the plasma/serum samples of 81% (13 of 16) of the cases. No methylated p16 sequences were detected in the peripheral plasma/serum of the six HCC cases without these changes in the tumor, in 38 patients with chronic hepatitis/cirrhosis, or in 10 healthy control subjects. These results suggest that circulating liver tumor DNA may be detected using tumor-associated DNA methylation changes. Because methylation abnormalities have been found in many other genes and tumor types, this approach may have implications for the noninvasive detection of a wide variety of cancers.

Adult↗
PubMed2004

Liver transplantation in transthyretin-related familial amyloid polyneuropathy.

PURPOSE OF REVIEW: Familial amyloid polyneuropathy (FAP) associated with mutations in the gene for transthyretin is a rare, progressively disabling and ultimately fatal inherited disease. Transthyretin is produced predominantly in the liver, and orthotopic liver transplantation (OLT) eliminates more than 95% of variant amyloidogenic transthyretin from the circulation. Liver transplantation remains the only potentially curative treatment in this disorder, but many recent studies have suggested that outcome following transplantation may be poorer than previously considered in some groups of FAP patients. RECENT FINDINGS: We review here the available data on the use and clinical outcome of OLT in patients with FAP, and consider the significance of particular mutations and cardiac amyloid involvement. The practice of combined organ transplants and domino liver transplantation is also reviewed. SUMMARY: Published data generally support OLT as a treatment for FAP, particularly in younger patients with the most prevalent transthyretin (TTR) Met30 variant, who have mild symptoms. Although excellent outcomes have been reported, including improvement in autonomic and to a lesser extent peripheral nerve function coupled with regression of visceral amyloid deposits, the results of OLT are influenced by many factors that include properties of particular transthyretin variants, nutritional status, age, severity of neuropathy and cardiac amyloid involvement. Paradoxical acceleration of transthyretin amyloid deposition following OLT may occur in the heart and certain other sites in some patients. The combination of kidney or heart transplantation with OLT may occasionally be appropriate. The long-term outcome of patients with FAP who have undergone OLT, and recipients of FAP domino liver transplants, remain to be determined.

Amyloid Neuropathies, Familial↗