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H Liehr

Publications and source records attributed to H Liehr.

At least 73 records · Page 4Linked to original sources

Significance of endotoxaemia in experimental "galactosamine-hepatitis" in the rat.

The course of galactosamine hepatitis induced by 1.0 g/kg i.p. injected galactosamine (Ga1N) was investigated a sequential study in normal rats, in colectomized rats, and in rats being endotoxin resistent against both exogenous and endogenous endotoxin. Clinical symptoms of Ga1N-hepatitis such as pyrogen reaction, disseminated intravascular coagulation, arterial hypotension, and hypoglycaemia correlated significantly with the development of endotoxaemia, which was detected by means of the limulus gelation test (L.G.T.) Ga1N refractoriness was found after colectomy, a situation, in which gram negative bacterias and their endotoxins were eliminated. Ga1N refractoriness was also observed in case of endotoxin resistence. It is concluded that endotoxins contribute significantly to the pathogenesis of "Ga1N-hepatitis" and its clinical symptoms.

Animals↗

[Morphological investigations of extrahepatic disorders after porta-caval end-to-side-anastomosis in rats (author's transl)].

Disorders of the central nervous system were found in 150 rats five monthds after en-to-side-porta-caval anastomosis consisting of vacuolisated cytoplasma of gangliacells and reactions of the glia comparable with the Alzheimer-glia-type II. Since these disorders are consistent with those in patients with liver cirrhosis but induced in these experiments by a porta-caval anastomosis alone, they are proposedly independent from liver disease itself. It is discussed whether disorders in glucose homeostai may be of pathogenetic relevance. Atrophy of tests, found in the late postoperative phase and erosions or ulcers of gastric mucosa as well as nephrolithiasis with hydronephrosis as consequence, the latter occuring independently from the time after operations, are proposedly due to the porta-caval anastomosis, too.

Animals↗

Hepatic blood flow and cardiac output after porta-caval anastomosis in the rat.

Investigations were performed in rats with portacaval anastomosis (PCA) in order to measure hepatic hemodynamics and cardiac output (CO) 3, 6, 14 and 28 days after operation under pentobarbitone anesthesia using the flow fraction distribution method (131I-MAA) of CO. The latter was calculated using Vierordt's principle from blood volume (BV) (125RIHSA-dilution method) and ICG-appearance time (ICG-AT) (ear-densitometry). Even 3 days after PCA CO was increased to 38.7 +/- 5.0 (SD) ml/min/100 g b.w. (normal 23.8), due to an increase of BV from 6.3 +/- 1.4 to 7.5 +/- 0.6 ml/100 g b.w. and a decrease of ICG-AT from 3.6 +/- 0.4 to 2.8 +/- 0.5 s. Arterial hepatic flow fraction of CO increased to 8.7 +/- 2.8% (control: 5.5 +/- 2.4%). Changes could be observed up to day 28. Hepatic blood flow per g liver tended to stabilize but was still decreased at day 28: 1.5 +/- 0.6 ml/min/g liver (control: 2.0 +/- 0.3). The typical hemodynamic changes in human liver cirrhosis can be reproduced by PCA alone. They are considered to be compensatory mechanisms for a reduced portal liver blood flow, which are not found to compensate completely.

Animals↗

Portal venous and systemic endotoxaemia in patients without liver disease and systemic endotoxaemia in patients with cirrhosis.

Systemic endotoxaemia without evidence of gram-negative bacterial infection occurs in liver diseases in man. The endotoxaemia is probably due to impaired hepatic clearance of endotoxin absorbed from the gastrointestinal tract, but portal venous endotoxaemia has never been reported in man. By means of the limulus gelation test, portal venous blood from 21 patients without parenchymal liver disease and arterial blood from 21 patients without parenchymal liver disease and 31 patients with cirrhosis was examined for endotoxin. Portal venous endotoxaemia was found in 9 of 21 samples and systemic endotoxaemia was found in 2 of 21 samples from patients without liver disease. Systemic endotoxaemia in cirrhosis occurred with a frequency of 15/31. No relationship to gram-negative bacteraemia was found. Leucocytosis was only seen in endotoxin-positive patients with cirrhosis. In cirrhosis higher levels of E. coli O antibodies were found in endotoxin-positive than in endotoxin-negative patients, supporting the view that the limulus gelation test specifically detects endotoxin (i.e. E. coli O antigen). The study suggests that endotoxin is a normal constituent of portal venous blood in man. The normal human liver clears endotoxin from the portal venous blood. This effect is diminished in cirrhosis, most probably owing to decreased phagocytic function of the liver. The increased humoral immune response in cirrhosis may be related to spillover of endotoxin from the liver.

Antibodies, Bacterial↗

[Effects of endotoxinemia on renal and intrarenal hemodynamics of rats with or without portacaval anastomosis].

Renal dysfunction in patients with cirrhosis of the liver is frequent especially in connection with endotoxaemia. Renal and intrarenal haemodynamics were investigated, therefore, in normal rats with or without portacaval anastomosis (PCA) by means of the cardiac output (CO) fractionation technique using microspheres. The intrarenal blood distribution was estimated after anatomical separation of renal cortex and medulla. In normal rats the total renal fraction of CO was 22.5 +/- 7.2%, and the renal medulla fraction 0.8 +/- 0.4% of CO. After a single injection of E. coli-endotoxin (1.5 mg/kg b.w.) the animals developed a high-cardiac-output state, the mean arterial pressure decreased from 110 +/- 15 mm Hg to 81 +/- 6 mm Hg. Renal fraction of CO was unaltered but the blood flow through the kidney was increased due to the high CO. The blood flow of the medulla increased five to tenfold of control values whereas renal cortical blood flow decreased. During the first eight hours after endotoxin administration the animals developed polyuria with a decrease of urine osmolality. Comparable systemic and renal haemodynamics were present in untreated PCA-rats, in which endotoxaemia was present spontaneously (Limulus Gelation Test). Additional endotoxin administration in these animals caused severe shock syndrome with a decrease in total renal perfusion and a further decrease in renal cortical blood flow. Endotoxin administration in normal rats caused minimal morphological alterations in the kidneys which were comparable with those found in PCA-rats. Endotoxin administration in PCA-rats however leads to severe damage of the kidney with fibrin deposits in the glomerula and acute tubular necroses. The haemodynamic, functional and morphological changes caused by endotoxin in the experiments are observed in principle in patients with cirrhosis of the liver too. This indicates that endotoxin should be taken into considerations concerning the pathogenesis of renal failure in patients with cirrhosis of the liver.

Animals↗

[Endotoxinemia in liver cirrhosis].

Endotoxins of gram-negative bacteria and of intestinal origin, insufficiently cleared by the hepatic reticulo-endothelial system are of an increasing interest within the pathogenesis of liver diseases. With purpose to obtain data concerning incidence and course of endotoxaemia in patients with liver cirrhosis an unselected group of these patients, sequentially admitted, was investigated by means of the Limulus-gelation test, regarded as most sensitive to endotoxins. At the admittance, 65% of the patients had endotoxaemia, further 14% developed endotoxaemia later. In total 79% of the patients investigated had endotoxaemia.---Bleeding from oesophageal varices was associated with endotoxaemia in 78%, functional renal impairment in 75%, consumption coagulopathy in 81%, encephalopathy in 77% and a pyrogen reaction in 82% of the patients. Regarding the Limulus assay, the dilution technique was more sensitive in detection of free endotoxaemia as opposed to the chloroform extract. It is concluded from the results that endotoxaemia in patients with liver cirrhosis is frequent and has to be viewed as relevant within the pathogeneses of chronic liver diseases.

Blood Coagulation Disorders↗