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J Lagarriga

Publications and source records attributed to J Lagarriga.

8 recordsLinked to original sources
PubMedDate not supplied

[Prevention of cholelithiasis with ascorbic acid. Experimental study in hamsters].

Cholesterol lithogenesis is the end result of hepatic microsomal enzymatic alterations which determine an increase in cholesterol synthesis (HMG CoA reductase) and a decrease in its transformation into bile salts (7 alpha hydroxylase). Therefore biliary cholesterol excretion is increased while bile salt excretion is diminished. Ascorbic Acid (A.A.) seems capable of reversing those enzymatic derrangements in scorbutic animals. Since hamsters are able to synthesize A.A., we evaluated its effect used in high doses during diet induced lithogenesis. Two groups of 6 weeks old, male hamsters, were fed with a lithogenic diet for 30 days. Group A received the usual amount of A.A. contained in the diet (0.25 mg/day/manster) while group B had supplementary A.A. added to drinking water (5 mg/day/hamster). Thirteen out of twenty of group A (65%) and 5 out of 20 of group B (25%) developed cholesterol calculi (p 0.05). Less stones were found in the gallbladders of hamsters fed with supplementary A.A. It is concluded that A.A. in this model, has an inhibitory effect on lithogenesis. The possible mechanism seems to be related to A.A. influence on the microsomal enzymes involved in lithogenesis. These findings, plus the lack of undesirable secondary effects of supplementary A.A. suggest a potential therapeutic role in human cholelithiasis.

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PubMedDate not supplied

[Hepatinecrosis caused by furosemide. Special lesions of various species?].

Furosemide is a wellknown hepatotoxic agent in rodents. Toxicity is result of the production of a catabolite by action of microsomal enzymes. The goal of this study was to demonstrate differences in toxicity between two rodents species: rat and hamster. Animals received 400 mg/k/i.p. of furosemide, with or without pretreatment with phenobarbital as enzymatic inducer. Adequates controls were used. Microscopic findings were different in both groups. Rats treated with furosemide plus phenobarbital, exhibited extensive mediozonal necrosis; when those without pretreatment, showed less extensive necrosis of liver cells, erratic in distribution. In contrast, it was a lack of necrosis in hamsters' livers, showing only unremarkable changes.

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