Biomedical subjects

W Murmann

Publications and source records attributed to W Murmann.

At least 37 records · Page 2Linked to original sources

PubMed1978

Effects of cicloxilic acid on CCl4-induced liver injury.

The effects of cis-2-hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) on the liver injury produced by carbon tetrachloride poisoning were studied in rats. It was found that oral treatment counteracts the CCl4-induced increase in liver weight, rise of liver triglycerides, fall of plasma triglycerides and rise of serum transaminase and ornithine carbamoyl transferase activities. Further, cicloxilic acid, when administered alone, altered none of the parameters studied. Cicloxilic acid was found to be more effective at the lowest doses than any of the other antihepatotoxic and choleretic drugs used. When cicloxilic acid was administered at the highest doses, the plasma triglyceride level of the intoxicated animals was not significantly different from that of the controls. To find out whether cicloxilic acid was effective in maintaining a normal lipoprotein secretion after CCl4 poisoning, experiments were carried out with Triton WR-1339. The results indicate that cicloxilic acid maintains the output of triglycerides from the liver to the plasma compartment at near-normal level in CCl4 poisoned rats. Possible mechanisms for the effects of cicloxilic acid on the CCl4-induced liver damage are discussed.

Animals↗

PubMed1978

Hepatic microsomal mixed-function oxidase system in rats pretreated with cicloxilic acid.

In a study of the hepatic microsomal drug metabolising system in rats, pretreatment with cis-2-hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) did not prolong pentobarbital sleeping time or decrease the cytochrome P 450 content of the liver microsomes. The drug interacted with the liver microsomes to yield a type II spectral change. Cicloxilic acid did not affect the metabolism of CCl4 in vivo, as judged by the covalent binding of 14C from 14CCl r to microsomal lipids, or delay the gastrointestinal absorption of CCl4, as judged by the concentration of free CCl4 in the liver. The protection afforded by cicloxilic acid against CCl4 liver damage is therefore due neither to inhibition of the metabolism nor to delayed absorption of the toxin.

Animals↗

PubMed1978

Effects of cicloxilic acid on secretory function of the liver. I. Effect on bile flow and on biliary secretion of bilirubin and glucuronic acid in anesthetised bileduct-cannulated rat.

Both in normal and experimentally jaundiced rats cis-2-hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) induces a greater and longer lasting increase in bile flow and a greater increase in bilirubin and glucuronic acid secretion than do the choleretics sodium 2-(2-hydroxy-3n hexoxy-propoxy)-benzoate and dehydrocholic acid. The intense increase in bilirubin secretion is interpreted as the outcome of stimulation of the biliary secretion mechanisms whilst the effect on bile flow and on the biliary secretion of glucuronic acid are attributed to the kinetics of biliary secretion of cicloxilic acid.

Anesthesia↗

PubMed1978

Effects of cicloxilic acid on secretory function of the liver. II. Effect on biliary secretion of bile acids, cholesterol and lecithin in anesthetised bileduct-cannulated rat.

cis-2-Hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) increases the output of bile acids and decreases that of cholesterol both in normal and in sodium taurocholate-infused rats; the biliary output of lecithin remains unchanged in normal animals but is increased in taurocholate-treated animals. The increased output of bile acids is interpreted as true stimulation of the bile-forming function of the liver, an activity supposedly mediated by stimulation of the metabolism of cholesterol to bile acids, independent of the drug's hydrocholeretic properties. The changes in the relative molar concentrations of the three micelle-forming bile constituents, namely bile acids, cholesterol, and lecithin, induced by cicloxilic acid lead to an appreciable lowering of the lithogenic index, thus suggesting that the drug may have antilithogenic activity.

Animals↗

PubMed1978