๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Acetaminophen-induced fulminant hepatic failure in Dogs

โœ Scribed by L. Ortega; J. I. Landa Garcia; A. Torres Garcia; G. Silecchia; J. Arenas; A. Suarez; M. Moreno Azcoitia; J. Sanz Esponera; E. Moreno Gonzalez; J. L. Balibrea Cantero


Publisher
John Wiley and Sons
Year
1985
Tongue
English
Weight
516 KB
Volume
5
Category
Article
ISSN
0270-9139

No coin nor oath required. For personal study only.

โœฆ Synopsis


Results concerning morphological and biochemical changes following intravenous administration of different doses of acetaminophen in dogs are reported. Acetaminophen infusion, as a parenteral solution (500 mg per kg per 90 min), produced fulminant hepatitis characterized by a good correlation between Portmann's grade of lesion and percentage of necrosis. All animals died within 76 hr after intoxication. Analysis of biochemical parameters revealed positive correlation between serum bilirubin levels and severity of the hepatic lesion. The experimental model of acetaminophen-induced hepatotoxicity is proposed as a model for evaluation of the therapeutic efficacy of new medical and surgical procedures.


๐Ÿ“œ SIMILAR VOLUMES


An improved model of acetaminophen-induc
โœ James H. Kelly; Tarek Koussayer; Da-Er He; Maria G. Chong; Thomas A. Shang; Hart ๐Ÿ“‚ Article ๐Ÿ“… 1992 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 920 KB

We have established an improved model of fulminant hepatic failure in dogs. Buthionine sulfoximine is used to inactivate glutathione synthesis, and small increments of acetaminophen are given intravenously to maintain the plasma level at approximately 200 pg/ml for 20 hr. This regimen produces sever

Histopathological heterogeneity in fulmi
โœ Cheryl Hanau; Santiago J. Munoz; Raphael Rubin ๐Ÿ“‚ Article ๐Ÿ“… 1995 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 1011 KB

The clinicopathological features of 38 patients admitted consecutively for fulminant hepatic failure were studied. Histopathological material was reviewed in all patients. Both percutaneous and whole livers (either explanted or autopsy specimens) were available in 16 patients: whole livers only in 1

Posttransplantation chronic hepatitis in
โœ R Mohamed; S G Hubscher; D F Mirza; B K Gunson; D J Mutimer ๐Ÿ“‚ Article ๐Ÿ“… 1997 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 942 KB

The incidence of chronic hepatitis in the overall liver trans-Specimens were processed routinely into paraffin blocks and stained with the following: hematoxylin and eosin, hematoxylin van Gieson, reticulin, orcein, Perl's reaction, and periodic acid Schiff with and without diastase pretreatment. Sp

Matrix metalloproteinase-9 in fulminant
โœ Lluis Palenzuela; Antoni Mas; Joan Montaner; Juan Cordoba ๐Ÿ“‚ Article ๐Ÿ“… 2010 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 304 KB

After reading the article by Taura et al. with great interest, we really appreciate the ingenious work they have done. 1 In this study, they found type I collagen-producing cells do not originate from hepatocytes in a triple transgenic mouse model. Hepatocytes in vivo neither express mesenchymal mar

Hepatocyte growth factor in fulminant he
โœ Robin D. Hughes; Christopher D. Gove; Roger Williams; Hirohita Tsubouchi; Yasush ๐Ÿ“‚ Article ๐Ÿ“… 1990 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 248 KB

We read with great interest the paper by Tsubouchi et al. (1) on the hepatocyte growth factor (hHGF) in the blood of patients with fulminant hepatic failure (FHF). These authors have already elegantly reported the purification and partial characterization of hHGF from the plasma of a patient with FH