PubMed Health⌕ Search

Biomedical subjects

U Rasenack

Publications and source records attributed to U Rasenack.

At least 19 recordsLinked to original sources
PubMed1983

[Angiomyolipoma of the kidney].

Upper abdominal ultrasound imaging in a 63-year-old woman who had been hypertensive for ten years revealed a tumour at the lower pole of the left kidney. It protruded from the renal surface and gave dense echoes, suggestive more of an angiomyolipoma than a hypernephroma. The former diagnosis was reenforced by the angiographic appearance and confirmed by biopsy at the time of surgery. Nephrectomy was performed and the postoperative course was without complication.

Angiography↗
PubMed1981

[Changes in the liver and brain after portacaval and modified portacaval end-to-side anastomosis: histology, autoradiography and clinical studies].

Histological studies were done in order to investigate the early and late alterations of the liver and brain in rats after establishment of portacaval anastomosis and modified portacaval anastomosis. The latter procedure allows pancreatic blood to flow into the liver beside portacaval anastomosis. Shunting of portal blood into the systemic circulation through a portacaval anastomosis resulted in hemo-dynamically induced central lobular necrosis of the liver. Necroses and atrophy were less pronounced after modified portacaval anastomosis. The results indicate that optimal perfusion and direct access of hepatotrophic factors are of great importance. Cell necroses in the late phase after portacaval anastomosis are possible due to endotoxinemia. Liver epithelial proliferation was markedly enhanced after complete shunting of portal blood into the systemic circulation. Only minimal proliferation was observed after modified portacaval anastomosis. The results cast doubt on the hypothesis of Starzl that hepatotrophic factors are necessary for all proliferation. Nodular hyperplasia occurring in the late phase of portacaval anastomosis may be due to proliferation of the epithelium. Necroses and injury of ganglia cells as well as alterations of the glia represent the morphological changes in portal-systemic encephalopathy. This is a frequent complication of spontaneous or surgical portacaval collateral circulation. Such changes can also be observed when portacaval anastomosis was constructed in otherwise healthy rats. Increased incorporation rates of 3H-thymidine into the glia were indication for enhanced proliferating activity. Efforts undertaken to maintain the pancreatic venous blood flow to the liver beside portacaval anastomosis resulted in significant diminuation of brain pathology. This happened although the grade of hyperammonemia was virtually identical in both settings. The interpretation is offered that access of the liver to hepatotrophic substances from the pancreas prevents portal-systemic encephalopathy in portacaval anastomosis which is in agreement with data published in the literature. The observation implies that in clinical action exclusively those surgical technics should be used by which the venous blood supply from the pancreas to the liver is maintained.

Animals↗
PubMed1980

Lactulose--a drug with antiendotoxin effect.

Lactulose (beta-galactosido-fructose) was found to have anti-endotoxin properties: 670 mg lactulose abolished the gelating activity of mg E. coli endotoxin on Limulus lysate in vitro. When lactulose was fed to rats (6.3 +/- 1.1 g/kg/day) over a period of 4 or 8 days before i.v. administration of 0.5 g/kg galactosamine, the liver damage that normally develops was prevented. Since galactosamine-induced necrosis of hepatocytes and inflammatory reaction of the liver are mediated by systemic endotoxemia of intestinal origin, an anti-endotoxin effect of lactulose was demonstrated in vivo. We suggest that lactulose might offer a therapeutic basis in clinical situations in which endotoxemia is of pathogenetic significance, such as certain gastrointestinal and liver diseases, shock states and gram-negative sepsis.

Animals↗
PubMed1980

[Problems of hepatoportal encephalopathy after portacaval anastomosis in the rat (author's transl)].

Necrosis and injury of ganglia cells as well as alterations of the glia represent the morphological changes in portal-systemic encephalopathy. This is a frequent complication of a spontaneous or surgical porta-caval collateral circulation. Such changes can also be observed when porta-caval end-to-side anastomosis (PCA) was constructed in otherwise healthy rats. Increased incorporation rates of 3H-thymidine into the glia were indication for enhanced proliferating activity. Efforts done to maintain the pancreatic venous blood flow to the liver beside PCA resulted in significant diminuation of brain pathology and function. The latter measured by EEG. This happened although the grade of hyperammonemia was virtually identical in both settings. The interpretation is offered that access of the liver to hepatotrophic substances (i. e. insulin) from the pancreas prevents portal-systemic encephalopathy in PCA which is in agreement with data of the literature. The observation implies that in clinical action exclusively those surgical techniques should be used by which the venous blood supply from the pancreas to the liver is maintained.

Animals↗
PubMed1978

Synergistic action of hepatocyte membrane defect and activated complement system in liver cell death--an experimental approach to fulminant hepatic failure.

The hypothesis was tested whether under the presence of a membrane defect of hepatocytes an activation of the complement system leads to massive liver cell necrosis. Low doses of galactosamine (50, 100, and 200 mg/kg) were administered to rats with and without an additional i.v. injection of sublethal doses of endotoxin (1.5 mg/kg). The latter was done in order to activate the complement system via the C3-bypath. Neither after doses of 50 mg/kg and 100 mg/kg nor after an additional administration endotoxin liver cell necrosis were observed. A dose of 200 mg/kg led to moderate liver cell necrosis, and when administered with endotoxin fulminant hepatic necrosis developed. The explanation was given that only after 200 mg/kg alterations of hepatocytes membranes were present, which prepare liver cells for complement mediated hepatocytolysis. In rats to which 1 g/kg galactosamine was given in addition to endotoxin it was demonstrated by immunohistology that the third component of complement was already fixed on hepatocyte plasma membranes at hour 3 and was accumulated within areas of necrotic liver parenchymal cells at hour 12. Thus, liver cell death is suggested as complement mediated if the membranes are altered. Clinical implications are given in concern of fulminant hepatic failure and an approach to effective treatment regims.

Animals↗