Energy state, glycolytic intermediates and mitochondrial function in the liver during reversible and irreversible endotoxin shock.

Metabolites of the energy and carbohydrate metabolism and mitochondrial function in the liver were compared in rats with reversible as well as with irreversible shock. 6 h after induction of shock there was a close correlation between the severity of shock and the energy state of the liver. Only rats with irreversible shock showed a marked deterioration in parameters of the adenylate system, whereas in animals with reversible shock the energy state remained at control levels. Liver glycogen and glucose stores declined similarly in all shocked rats. The capacity of isolated liver mitochondria to produce ATP did not essentially differ in reversible and irreversible shock. Further investigations should consider the intracellular environment in evaluating the mitochondrial function in vivo during endotoxin shock.

[In vitro effects of E. coli endotoxin on the membrane permeability and substrate transport of isolated rat liver mitochondria]. / In vitro-Effekt von E. coli-Endotoxin auf Membranpermeabilität und Substrattransport isolierter Rattenlebermitochondrien.

Incubation of freshly isolated rat liver mitochondria with E. coli endotoxin resulted in an increased inner membrane permeability for K+ and Cl- ions. This effect was not prevented by addition of the synthetic antioxidant butylated hydroxytoluene. The carrier-mediated transport rates of phosphate, pyruvate, citrate and reducing equivalents via the malate-aspartate shuttle were not altered significantly by endotoxin. Therefore, the endotoxin-mediated impairment of mitochondrial respiration and oxidative phosphorylation could not be attributed to a decrease in transport capacities through the inner mitochondrial membrane.

Kinetic aspects of enzyme activity changes in blood plasma during canine hemorrhagic shock.

The kinetics of the increase in activities of eight enzymes in plasma was investigated in hemorrhagic shock in dogs (8.0 kPa, 120 min). The time-course of enzyme activity changes in shock differed between animals and depended on their sensitivity to shock. In the shock-sensitive group of dogs an exponential activity increase was already observed in the hypotension period. However, the dogs of the less shock-sensitive group showed a delay of enzyme release with significantly less pronounced elevation of all enzyme activities except creatine kinase. The initial exponential rise of enzyme activities, which approximately followed first-order kinetics, was quantitatively characterized by the release rates. There was a close correlation between the molecular weights of enzymes and their release rates during shock in both groups of dogs. The relevance of the results to mechanisms of enzyme transport from the cell into the blood is discussed.

[Biochemical and ultrastructural changes of the liver during the loss of cerebral function]. / Biochemische und ultrastrukturelle Veränderungen der Leber bei zerebralem Funktionsausfall.

Biochemical and electron optical changes in the liver cell were recorded at the experimental brain death in dogs. The investigation results refer to a hypoxic lesion at the beginning of the brain death despite of a strong flow in the hepatic artery and the portal vein. An enlarged shunt flow is discussed to be the cause.--A distinct recovery tendency shows the morphological picture at the state of the brain death despite reducing the hepatic blood-flow and without aimed therapeutic measures. This recovery tendency appears better in the electron microscopical finding than in the behaviour of the cell metabolites.