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Biomedical subjects

H Liehr

Publications and source records attributed to H Liehr.

At least 55 records · Page 3Linked to original sources
PubMed1979

[Percutaneous transhepatic--versus endoscopic retrograde cholangiography in the differential diagnosis of cholestasis? (author's transl)].

Since the introduction of the Chiba needle the percutaneous transhepatic cholangiography (PTC) became an established method in the differential diagnosis of cholestasis beside the endoscopic retrograde cholangiography (ERC). From the clinical point of view it is sometimes difficult to decide which of these two techniques should be preferred. In case of absolute or relative contraindications or in case of failure of one of the two methods ERC and PTC can be used alternatively. In all other cases we feel that the PTC by means of the Chiba needle is superior because of easier technical handling and higher success rate. In addition PTC is less trying for the patients. However on the basis of our own experience is should be stressed, that even by using skinny needles there is danger of bile leakage, which necessitates an immediate surgical intervention in the presence of biliary obstruction.

Cholangiography↗
PubMed1978

On the pathogenesis of galactosamine hepatitis. Indications of extrahepatocellular mechanisms responsible for liver cell death.

In order to evaluate the pathogenesis of galactosamine hepatitis, the action of galactosamine on mast cells, and alteration in the complement system suring the course of this experimental injury were studied. It has been previously demonstrated that rat livers after colectomy are refractory to galactosamine-induced liver cell necrosis and inflammation. For this reason colectomized animals were used to see whether the biochemical alterations produced by this aminosugar and thought to be responsible for cell death developed. Results showed: 1. galactosamine potently degranulates mast cells in vivo and in vitro, 2. the complement system is a) activated during the course of galactosamine hepatitis, probably by circulating endotoxins, and b) is essential for liver cell death in galactosamine hepatitis, and 3. colectomy does not prevent biochemical changes known to occur during galactosamine metabolism. It is concluded that death of galactosamine-injured liver cells is triggered by extrahepatocellular mechanisms, which lead ultimately to an activated complement system by endotoxins. It is postulated that related mechanism may also occur in viral hepatitis and in fulminant hepatic failure in man.

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↗
PubMed1978

[Clearance of antigens by the liver (author's transl)].

The liver is not only a metabolic organ, but has also immunological properties provided by the Kupffer cells which represent the major part of the body phagocytizing capacity. In case of an impairment of this function intestinal antigens, e.g. endotoxins, may reach the systemic circulation and thus exhibit their biological properties. The function of Kupffer cells obviously depends on a slow sinusoidal blood stream which latter is provided by blood flowing to the liver via the portal venous tract. This fact may be of consequence in porto-caval shunt surgery in order to use methods by which a rest flow through the portal vein to the liver is maintained. Thus, the organism is prevented from the biological consequences of an altered phagocytic function of the liver.

Antigens↗
PubMed1978

[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)].

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.

Blood Coagulation Disorders↗
PubMed1977

[Significance of liver volume for the early survival of patients with liver cirrhosis operated on porta-caval anastomosis: Clinical data and relation to pathophysiological implications (author's transl)].

It is thought that the early outcome of patients with liver cirrhosis after end-to-side porta-caval anastomosis not only depends on their clinical situation but also on the postoperative haemodynamic state of the liver. The postoperative haemodynamics can be estimated if the relation of liver volume and the predicted hepatic arterial perfusion is focused. The maximum of arterial liver perfusion seems to be 1200 ml/min in the absence of a portal liver blood supply. Thus, a postoperative perfusionindex between 0.8-1.2 like in normal subjects seems to be the best situation to prevent postoperative hepatic underperfusion. 25 patients were investigated, in which the clinical situation was classified as recommended by Child, and liver volume was estimated by means of ultrasonography. Those patients having liver volumes between 1000 and 1500 ml providing a postoperative PI between 0.8-12 survived in 100%. The early mortality rate of those, having liver volumes more or less these thresholds died in 69%. It was concluded that hepatomegaly or extreme liver atrophy are situations not to be recommended for classical porta-caval anastomosis. Other procedures are dissussed which "seem to be some good news" by clinical data and by means of experimental results. The techniques discussed consist in procedures preventing the pancreatic venous blood to shunt away from the liver.

Adult↗
PubMed1977

[Effects of porto-caval end-to-side-anastomosis on the liver of rats (author's transl)].

In young rats (n = 117), with a liver weight of 9.9 +/- 1.6 g ("small livers"), the decrease of total liver blood flow was followed by necrosis of liver parenchymal cells in the first two postoperative weeks. These alterations induced by haemodynamic disorders occured since the hepatic artery-although dilated to its maximum--was insufficient to compensate completely for the decrease of the portal hepatic blood flow. In old rats (n = 33) with a liver weight of nearly the double (19.5 +/- 1.9 g; "big livers") the extrem haemodynamic situation after PCA with a more less sufficient arterial hepatic blood supply was followed by complete liver necrosis including necrosis of the v. Kupffer cells. Rats having survived the PCA-operation showed liver cell necrosis in a more less degree as opposed to the early changes. These changes were not thought to be due to persisting haemodynamic disorders but due to endotoxaemia as found in 85% of the animals by means of the Limulus Gelation Test.

Animals↗
PubMed1977

[Angiographic studies of kidney failure in endotoxinemia].

Exogeneous endotoxaemia caused vasoconstriction of the juxtaglomerular arteries in otherwise healthy minipigs. This supports the view that reduced renal cortical blood flow in patients with liver disease can be caused by endotoxin. After portocaval anastomosis the efficacy of the liver RES to clear endotoxin was decreased due to the haemodynamic disorder. Thus, a dose of endotoxin, which was sublethal to healthy animals, became lethal owing to decreased RES-function. The increased endotoxin toxicity leads to a Shwartzman-Sanarelli-reaction. A dose of toxin which caused death in all animals with a portocaval shunt alone was not lethel in any animal in which an arterialization procedure was simultaneously performed, suggesting a possible improvement of RES function. These findings are of clinical importance for patients with renal failure in liver cirrhosis and hepatic failure. They suggest that endotoxaemia is of pathogenetic relevance in the development of functional renal failure.

Animals↗