[The biotransformation of inhalation anaesthetics and its relevance to clinical side effects (author's transl)].

The volatile anesthetics are not inert substances, but they are metabolised by means of a non-specific drug metabolizing enzyme system of the liver. Thus, in combined administration of several drugs, the knowledge of the metabolic pathways and the influence of the anesthetics on the transforming system is not only theoretically important, but represents a conditio sine qua non to the anesthesist as regards the handling of modern anesthetics. The occasionally observed liver and kidney injuries indicate a potential formation of toxic metabolites.

Ultrastructural evidence of the hepatotoxic effect of halothane in rats following in-utero exposure.

Eight pregnant Sprague-Dawley rates were exposed to 10 ppm halothane 8 hours/day and 5 days/week throughout pregnancy. Liver samples were obtained from the pups for electron microscopy. Degenerative changes such as myelin-figure formation, focal-cytoplasmic degradation; fatty changes and cellular necrosis were observed.

[Swelling and loss of potassium in perfused livers following the influence of the vapours of carbon tetrachloride, chloroform and halothane on the perfusion medium (author's transl)].

Erythrocyte free perfused rat livers were treated with vaporous carbon tetrachloride, chloroform and halothane by equilibration in the oxygenator system. The potassium loss, the amount of swelling and the alteration of the perfusion rates were measured during the experiments as criteria of acute toxicity. In contrast to the well known behaviour of perfused livers during the intoxication with phalloidin the amount of liver swelling did not marekdly depend on the perfusion rates in acute CCl(4) poisoning.

[Liver-damaging action of halothane--an animal experiment study].

After long-term exhibition to halothane (up to 96 hours), centrolobular hepatic damage (fatty degeneration, necrobiosis and necrosis) developed in rats, proportionally to the number of anesthesias and shortening of the intervals. From these results no hepatotoxic effect of halothane can be derived, since the alterations might be caused by hypoxia alone.

[Phalloidin antagonists 4th communication: Thioctic acid, SH-compounds, rifampicin, choleretics, dexamethasone, estradiol, unspecific inhibitors, and ineffective compounds (author's transl)].

1. Thioctic acid used clinically in poisoning by A. phalloides, protected perfused livers and also isolated hepatocytes against phalloidin, when given in high concentrations.

Halothane hepatitis with renal failure treated with hemodialysis and exchange transfusion.

A 38-year-old white female, hepatitis B antigen negative, developed fluminating hepatic failure associated with oliguria and severe azotemia after two halothane anesthesia and without exposure to other hepatotoxic drugs or blood transfusions. She was treated with multiple hemodialysis and exchange blood transfusion. The combined treatment corrected the uremic abnormalities and improved her level of consciousness.