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R Viebahn

Publications and source records attributed to R Viebahn.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Contrast-enhanced MR cholangiography in percutaneous bile duct drainage].

PURPOSE: To evaluate MR-cholangiography after instillation of contrast media via indwelling biliary tubes. METHODS: In 8 patients with stenoses of the central bile ducts, physiological saline solution and diluted contrast media (Gd-DTPA, 5 mmol/l) were consecutively administered via an indwelling biliary tube. MR cholangiograms were obtained before and after saline injection using a HASTE-sequence and after administration of Gd-DTPA using a T1-weighted gradient echo sequence. RESULTS: Peripheral bile ducts were better visualised in the water-sensitive approach than after Gd-DTPA enhancement. In patients with short-time drainage bile duct definition was poor due to periportal oedema. Visualisation of peripheral bile ducts could be improved by injection of saline solution in these patients. After administration of Gd-DTPA via the biliary tube contrast enhancement of the central bile ducts was achieved in all patients except for one patient on long-term drainage with an indwelling Yamakawa tube. CONCLUSION: T1-weighted visualisation of the central bile ducts can be achieved by means of injection of Gd-DTPA via indwelling biliary tubes.

Adult↗
PubMed1996

TCDD-inducible plasminogen activator inhibitor type 2 (PAI-2) in human hepatocytes, HepG2 and monocytic U937 cells.

Induction of PAI-2 by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been studied in human primary hepatocytes, hepatoma HepG2 cells and monocytic U937 cells, extending recent findings in human keratinocytes. PAI-2 represents a serpine-type protease inhibitor with wide-ranging implications in fibrinolysis, extracellular matrix proteolysis, growth factor activation and carcinogenesis. PAI-2 was induced by >10(-9) M TCDD in hepatocytes and HepG2 cells and by >10(-10) M TCDD in U937 cells. In the latter cell line, PAI-2 induction by TCDD and by 12-O-tetradecanoyl phorbol-13-acetate (TPA) has been compared. TCDD appeared to be less efficient than TPA as an inducer of PAI-2. In contrast to induction by TPA, PAI-2 induction by TCDD was found to be biphasic, with an early peak of mRNA at 1-3 h and a late peak at 12-24 h. A biphasic response was also seen at the protein level although production of PAI-2 protein lagged behind the corresponding mRNA. PAI-2 is known to contain AP-1 sites, i.e. Jun/Fos protein-binding sites, in its promotor region. Hence, PAI-2 induction by TCDD has originally been conceived to be due to an indirect response, secondary to the induction of Jun/Fos proteins. Therefore, expression of jun/fos genes and their AP-1 activity were studied at the early phase of PAI-2 induction by TCDD. TCDD did not increase mRNA of c-fos, c-jun, junB or junD (in contrast to TPA which markedly increased the expression of c-fos and junB), nor did TCDD increase AP-1 activity. In conclusion, the findings suggest that PAI-2 induction by TCDD is not restricted to human keratinocytes but includes liver cells and monocytic U937 cells. The induction mechanism is complex but the early phase does not appear to involve Jun/Fos proteins.

Aryl Hydrocarbon Receptor Nuclear Translocator↗
PubMed1996

[Does piggy-back liver transplantation have a detrimental effect on venous drainage?--A comparative duplex ultrasound study].

Venous drainage in "Piggy-back" Liver Transplantation "Piggy-back" orthotopic liver transplant (OLT) may offer some advantages (hemodynamic stability without veno-venous bypass) over standard OLT, but there is concern about the risk of venous outflow obstruction associated with this technique. In this study (n = 19 piggy-back, n = 12 standard OLT) it was possible to show, by means of duplex scanning, that flow velocity, resistance and flow of hepatic veins do not differ significantly.

Adult↗
PubMed1995

Induction of CYP1A and glutathione S-transferase activities by 2,3,7,8-tetrachlorodibenzo-p-dioxin in human hepatocyte cultures.

Induction of CYP1A and glutathione S-transferase activities with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in human hepatocytes in primary culture to investigate the variability of inducibility and the potency of TCDD. Determining induction of 7-ethoxyresorufin O-deethylase activity, preferentially catalyzed by CYP1A isozymes, we obtained concentration-response diagrams in TCDD-treated hepatocyte cultures from transplant donors and patients undergoing hepatic surgery. At a concentration of 10(-10) M TCDD approximately half-maximal induction of CYP1A was observed. Northern analysis of CYP1A gene expression showed a similar concentration-response relationship. In comparison with rat hepatocytes, human hepatocytes were about 10-fold less sensitive towards the CYP1A-inducing effect of TCDD. No pronounced interindividual differences in the inducing potency of TCDD (concentration which leads to half-maximal induction) were obvious in the six human individuals studied, whereas the efficacy of CYP1A induction was highly variable. In addition, inducibility of glutathione S-transferase (GST) activity also revealed a considerable degree of interindividual variation, i.e. a complete lack of induction in three out of six hepatocyte preparations and a highly variable efficacy of GST induction among responders which was not related to CYP1A inducibility.

Adult↗
PubMed1994

MHC antigen presentation on the surface of hepatocytes: modulation during and after hypoxic stress.

Presentation and recognition of MHC antigen on the surface of cells is the basic process of initiating rejection and distinguishing "self and not self". This is considered to begin when a transplanted organ is reperfused with the blood of the recipient. In this study, the modulation of MHC I antigen presentation during preservation was investigated in a cell culture model using primary hepatocyte cultures of male Wistar rats. By incubation with different preservation solutions used in clinical transplantation, expression of the MHC antigen was observed during cold hypoxia. Primary hepatocyte cultures were isolated from male Wistar rats by a modified Seglen technique and seeded to glass slides, thus obtaining monolayer cultures. After 1 day of resting the cultures were incubated under different conditions using Krebs Henseleit solution (KH), Euro-Collins solution (EC), HTK solution of Bretschneider (HTK) and University of Wisconsin solution (UW) as incubation media. The conditions of incubation were warm normoxia (37 degrees C, pO2 100 mm Hg) and cold hypoxia (4 degrees C, pO2 < 0.1 mm Hg), which is the main condition of organ preservation. Incubation time was 6 h. Before starting the incubation reference cultures were fixed and every 60 min several cultures were withdrawn from the experiment and fixed also. MHC expression was studied by staining the cultures with monoclonal antibodies against rat MHC class I and class II. As expected, MHC class II was not present on the surface of hepatocytes, while MHC class I was demonstrated on the controls as well as on the cultures that were incubated using KH and EC independent of temperature and hypoxia or normoxia. At the end of the incubation they were still positive but not as strong as in the beginning. During incubation using HTK and UW, MHC I was not detectable at all phases of the experiment. In conclusion, hypoxic stress did not completely eradicate MHC I expression in rat hepatocytes, while the composition of the preservation medium may result in a hepatocyte surface negative for MHC I. Hydroxyethylstarch may be the substance in UW that covers the MHC antigen, while in HTK, mannitol or the histidine complex may play the same role. MHC negativity of the cells of a preserved transplant is another reason for the benefit of UW or HTK.

Animals↗
PubMed1994

Preservation studies using acinar cell cultures of the pancreas: stimulation of amylase/lipase release before and after hypoxic stress.

In clinical pancreas transplantation, postischemic (i. e. postpreservation) transplant pancreatitis is a major problem in some cases but also an interesting model of pancreatitis. In this study, the effect of simulated organ preservation of isolated acinar cells was evaluated as regards enzyme release (basic and cerulein-stimulated), using common preservation solutions as the incubation media. Primary pancreas acinar cell cultures were isolated from the pancreas of male Wistar rats using the modified method of Amsterdam and Jamieson. After resting the cells in culture flasks for 1 week, monolayer cultures were obtained. The basic enzyme release of amylase and lipase was measured as well as the effect of stimulation with cerulein (10(-8) M) and the effect of replacing the medium (without changing the consistence or temperature of the medium). In a second step, the cultures were incubated under conditions of cold hypoxia for 6 h (4 degrees C, P O2 < 0.1 mm Hg) using Krebs-Henseleit solution (KH), Euro-Collins solution (EC), HTK solution of Bretschneider (HTK) or University of Wisconsin solution (UW) as the incubation solution. After 6 h, the media were changed to warm normoxic KH, and a second stimulation test with cerulein was performed. The native microstructure of the cultures was observed as well. Enzyme release was elevated by a factor of 5 by stimulating the acinar cells with cerulein as well as by changing the medium in the experiments prior to the hypoxic incubation. After hypoxic incubation and change to KH, the morphology of the cultures was excellent, while the basic enzyme release was on a very low level, no matter which preservation solution was used during cold hypoxia. Stimulation with cerulein caused only minimal elevation of enzyme release during an observation period of 60 min. These observations show that cold storage in preservation solution provides maintenance of the cell morphology and sufficient down-regulation of enzyme release of pancreatic acinar cells. Thus, acinar cells alone do not seem to be the pacemaker of pancreatitis after organ preservation. The presented experimental model will be the subject of extended evaluation in the future.

Amylases↗
PubMed1994

[Liver resection in hepatocellular carcinoma].

Hepatic resection offers the only chance of cure for patients with hepatocellular carcinoma. Preoperative tumor staging is based on radiologic procedures (ultrasound, CT- and MR-imaging). Compromised hepatic function will limit resectability, leaving only palliative procedures. Unfavorable prognostic tumor factors (diameter > 5 cm, multifocal, nonencapsulated, vascular invasion) should lead to a combination of adjuvant chemotherapy/chemoembolization and surgical intervention. In irresectable situations multimodality treatment protocols (combined i.v. chemotherapy, radio-immuno-therapy) play an increasing role.

Carcinoma, Hepatocellular↗
PubMed1994

[Therapeutic interventional radiology procedures in hepatocellular carcinoma].

Interventional treatment of hepatocellular carcinoma is indicated if surgical treatment is impossible. Selection of the individual method of interventional treatment is determined by the size, location and number of tumors and by the grade of tumor vascularization. Tumors below 5 cm in diameter are well-suitable for aethanol ablation. In larger tumors and in tumors with high-grade vascularization transarterial chemoembolization is probably more effective. In patients with more than 3 tumor nodules chemoembolization is the treatment of choice. On the other hand chemoembolization shows reduced efficacy in tumors with low-grade hypervascularization and the aethanol ablation as a stand-alone procedure or supplemental treatment seems to be valuable. Until now there is no generally accepted opinion in terms of the indications for different methods of interventional treatment. Further comparative studies including aethanol ablation, chemoembolization and resection are necessary.

Carcinoma, Hepatocellular↗
PubMed1994

The potential role of reactive oxygen species in liver ischemia/reperfusion injury following liver surgery.

Reperfusion of a previously ischemic tissue may lead to an aggravation of injury. The liver has been shown to be susceptible to this reperfusion injury in several experimental systems. Reactive oxygen species appear to play an important role in the development of such injury, as has been demonstrated by direct measurements of their release, and by the protective effects of antioxidants. Upon reperfusion, reactive oxygen species may be released by hepatocytes, Kupffer cells and neutrophils. The relative contribution of the various liver cell types to the release of reactive oxygen species depends on several factors, including the duration and condition of ischemia and the time elapsed after reperfusion. There is only limited evidence for the occurrence of reperfusion injury in humans following liver surgery. The role of reactive oxygen species in this injury in humans remains to be shown.

Animals↗
PubMed1994

[Liver transplantation in halothane-induced liver necrosis].

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.

Adult↗
PubMed1993

[Acute cholecystitis in a traumatologic patient sample].

Among the patients of the Accident Hospital of the Co-operative Trade Association Tübingen, there were 11 cases of acute cholecystitis between 1985 and 1991. Acute cholecystitis occurred after polytrauma (n = 5), multiple fractures (n = 2), head injury (n = 1), fracture of femoral neck (n = 1) or elective hip surgery (arthrodesis, total hip replacement) (n = 2). The mean age was 57 (16-89) years, acute cholecystitis was confirmed 27 (6-54) days after trauma of surgery. 7 cases presented as acute acalculous cholecystitis, whereas in 4 cases of acute cholecystitis cholecystolithiasis was present. 9 patients were treated via cholecystectomy; one juvenile paraplegic recovered after conservative treatment, one 82-year old female was in too bad condition for surgery so that percutaneous cholecystostomy had to be performed prior to cholecystectomy. 10 patients recovered without complication, one 89-year old multi-morbid male died after cholecystectomy. Analysis of the clinical course prior to the occurrence of acute cholecystitis showed a high incidence of shock, frequent blood transfusion, long-time respiratory therapy and parenteral nutrition as well severe trauma, and high cumulation of opiate therapy in this group of patients. Diagnosis was confirmed by ultrasound in all patients, clinical symptoms and laboratory data being mostly unspecific.

Adolescent↗
PubMed1991

[Primary hepatocyte cultures as a model of experimental study of liver preservation].

Primary hepatocyte cultures have been used to evaluate data concerning hypoxic liver cell injury. To show the suitability of this method in liver preservation studies hepatocyte cultures were incubated under different conditions: warm normoxia (37 degrees C, pO2 greater than 70 mm Hg), warm hypoxia (37 degrees C, pO2 less than 0.1 mm Hg), cold normoxia (4 degrees C, pO2 greater than 70 mm Hg) and cold hypoxia (4 degrees C, pO2 less than 0.1 mm Hg). Incubations were performed in Euro Collins solution (EC), University of Wisconsin solution of Belzer (UW) and histidine ketoglutarat tryptophan solution of Bretschneider (HTK) as well as in Krebs Henseleit buffer (KH) for control incubations. During 12 h of incubation hepatocyte cultures under warm normoxia lost viability continuously in EC, UW and HTK while in KH they remained stable. Under warm normoxia all cultures lost 50% of their viability during 12 h of incubation while in cold normoxia loss of viability was mild but significant. Under cold anoxia which is the standard condition of liver preservation the cultured hepatocytes remained unchanged for 12 h in KH, UW and HTK, while in EC most of the cells were dead after 6 h. It is concluded that incubations of primary hepatocyte cultures under different pO2 and temperatures are well suited to contribute to liver preservation studies on a preclinical level and thus may help to save animal experiments.

Animals↗
PubMed1991

Differences in glycolytic capacity and hypoxia tolerance between hepatoma cells and hepatocytes.

Viability, glycolytic capacity and energy metabolism under anaerobic conditions were studied in the hepatoma cell lines HTC, FU5 and HepG2 and in rat and human hepatocytes using glucose and fructose as glycolytic precursors. During 6 hr of anaerobic incubation without additional substrate, viability decreased rapidly in FU5 and HTC cells, whereas viability of HepG2 cells was not significantly affected. In all tumor cells, 10 mmol/L glucose prevented hypoxic cell injury almost completely. Lactate formation from glucose was about five times higher than in hepatocytes under these circumstances. ATP content of the tumor cells remained almost constant under anaerobic conditions in the presence of glucose. Ten millimoles per liter of fructose diminished glycolysis in the hepatoma cells compared with glucose, ranging from 87% reduction in HTC cells to 43% reduction in HepG2 cells. Accordingly, ATP content decreased rapidly in the FU5 and slowly in the HepG2 cells. Viability was strongly diminished in the HTC and FU5 cells in the presence of fructose, whereas in the HepG2 cells no effect of fructose on viability was detectable. In contrast to the hepatoma cells, rat and human hepatocytes exhibited higher rates of anaerobic glycolysis in the presence of fructose and thus were able to maintain their viability under these conditions. These differences in glycolytic capacity, energy metabolism and hypoxia tolerance of hepatoma cells compared with hepatocytes may be used for the treatment of liver cancer by isolated liver perfusion and ex situ revision of the organ.

Adenosine Diphosphate↗