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Biomedical subjects

H Liehr

Publications and source records attributed to H Liehr.

At least 91 records · Page 5Linked to original sources
PubMed1975

Endotoxin-induced liver necrosis and intravascular coagulation in rats enhanced by portacaval collateral circulation.

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.

Alanine Transaminase↗
PubMed1975

Galactosamine- "hepatitis" in rats with different phagocytic activity of liver RES.

Morphological investigations by lightmicroscopy were performed to evaluate the influence of an altered liver RES-function state on the course of Gal-N-hepatitis. There was a good correlation between the biochemical data and the morphological alterations. The simultaneous infusion of Gal-N 1 g/kg b.w. and carbon particles (2.6 mg/100 g b.w) into the portal vein was followed by subtotal necrosis of the liver and Sanarelli-Shwartzmann-phenomenon. Signs of RES-activity were nearly absent. 8 days after pretreatment with carbon, Gal-N application did not produce Gal-N hepatitis; 21 days after carbon infusion the morphological changes normally found after Gal-N application were present. The morphological studies confirm the concept that an altered RES-function state is a very important factor for the development of liver cell necrosis.

Animals↗