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Biomedical subjects

M Frimmer

Publications and source records attributed to M Frimmer.

At least 73 records · Page 4Linked to original sources
PubMed1975

[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. The mechanism of swelling must be different in both intoxications. Exposure of perfused livers to high concentrations of CCl(4) for several minutes only produced a marked K-+-loss within a short time. This injury could not be fully compensated after finishing the exposure. Dose response diagrams are presented for carbon tetrachloride, chloroform and halothane by use of the following criteria: potassium loss, swelling (increase of wet weight) and perfusion rates (ml.min-1.g-1). As total doses the amounts of solutes vaporized during the exposition were listed. In these diagrams chloroform appears to be more toxic than halothane. CCl4 occupies a middle position between chloroform and halothane. The course of dose response diagrams of halothane is different from those of CCl(4) and CHCl(3). The halothane diagrams increase critically at high doses, whereas the courves for CCl(4) and CHCl(3) rise continuously. With respect to effects on the hepatic microcirculation halothane seems to be less toxic than CCl(4). The results are discussed on the basis of the periods of exposition and the maximal concentrations of the solutes in the perfusion medium. With respect to these data CCl(4) is much more toxic than CHCl(3) and halothane. On the other hand there is no marked difference in acute hepatotoxicity between CHCl(3) and halothane.

Acute Disease↗
PubMed1975

[Phalloidin antagonists/3rd communication: effects of antamanide derivatives in isolated perfused rat livers (author's transl)].

The protective effects of antamanide, O-carboxy-methyl-Tyr5-antamanide and of Tyr6-antamanide-monosulfate against phalloidin were tested in perfused rat livers. None of the applied doses was able to inhibit swelling and potassium loss of poisoned livers completely. In the perfused liver antamanide preferentially inhibited swelling but not potassium loss. O-Carboxymethyl-Tyr5-antamanide protected isolated hepatocytes against phalloidin. The different effects of antamanide derivatives in perfused livers and in vivo are discussed.

Animals↗
PubMed1975

[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. 2. Some SH-compounds like coenzyme A, dimercaprol, cysteine and cysteamine were found to be protective in different concentrations. 3. Rifampicin protects mice against lethal doses of phalloidin, and inhibits poisoning of isolated hepatocytes at low concentrations. 4. Some choleretic drugs like dehydrocholate, temoebilin (extr. cucumae xanth.), ethacrynic acid influenced phalloidin poisoning by inhibition of binding. 5. Doses of 0.2 to 4.0 mg dexamethasone added to 100 ml of perfusion medium did not protect perfused rat livers against 0.5 mg phalloidin. 6. Pretreatment of female rats with estrogens effected protection against phalloidin in vivo. The same procedure resulted in moderate decrease of phalloidin effects when the livers of pretreated animals were poisoned in vitro. In male rats estrogen pretreatment was less effective. Castration did not augment the protective effect. 7. Secophalloidin, a biologically inactive derivative, did not influence phalloidin poisoning in perfused livers, even when applied in excessive concentrations. 8. Concanavalin A, probably bound in the neighborhood of binding sites for phalloidin, did not protect perfused livers against phalloidin. 9 Diethyldithiocarbamate, a compound protecting livers against carbon tetrachloride and halothane, was ineffective in phalloidin poisoning. 10. Further protective actions of Evans blue, of some phenanthrolines and of EDTA are discussed. 11. Pretreatment of animals with hepatotoxic compounds (CCl4, CHCl3, cinchophen) decreased the toxicity of phalloidin in vivo. Possible mechanisms are discussed.

Animals↗