“…Animal model of FHF induced by surgical methods, including hepatectomy and ischemic models, seems not suitable for testing the efficacy of a BAL device because they lack potential reversibility. Studies demonstrated that D-galactosamine induced FHF model possessed high reproducibility and potential reversibility, which met the majority of the criteria set by Terblanche and Hickman [32,36]. Moreover, this kind of animal model is morphologically similar to virus-or drug-related hepatic failure in human beings, as it is associated with neurological deterioration, hypoglycemia and death from liver failure [37][38][39].…”
Section: Discussionmentioning
confidence: 91%
“…FHF was induced in Buloc breeding pigs with intravenous administration of D-galactosamine (Sigma-Aldrich Inc., USA) as described elsewhere [32]. Briefly, after a 6 h fasting, anesthesia was achieved with intramuscular administration of Ketamine (4 mg/kg), muscle relaxation was obtained with intravenous administration of Vecuronium Bromide (2 mg/kg).…”
“…Animal model of FHF induced by surgical methods, including hepatectomy and ischemic models, seems not suitable for testing the efficacy of a BAL device because they lack potential reversibility. Studies demonstrated that D-galactosamine induced FHF model possessed high reproducibility and potential reversibility, which met the majority of the criteria set by Terblanche and Hickman [32,36]. Moreover, this kind of animal model is morphologically similar to virus-or drug-related hepatic failure in human beings, as it is associated with neurological deterioration, hypoglycemia and death from liver failure [37][38][39].…”
Section: Discussionmentioning
confidence: 91%
“…FHF was induced in Buloc breeding pigs with intravenous administration of D-galactosamine (Sigma-Aldrich Inc., USA) as described elsewhere [32]. Briefly, after a 6 h fasting, anesthesia was achieved with intramuscular administration of Ketamine (4 mg/kg), muscle relaxation was obtained with intravenous administration of Vecuronium Bromide (2 mg/kg).…”
“…The former includes hepatic ischemia and hepatectomy, and the latter are based on administering drugs and toxins, such as acetaminophen, D-galactosamine, azoxymethane, concanavalin A, and thioacetamide [37,38]. Our study adopted a widely accepted ALF porcine model induced by D-galactosamine [39,40] because this model demonstrates high reproducibility and potential reversibility [30][31][32]41]. Notably, this pig model was highly similar to both clinical and laboratory indices of patients with drug-induced ALF and provided a suitable model to evaluate the efficacy of our novel Li-ALS treatment.…”
“…This review discusses two of the more widely used hepatotoxins, galactosamine [29][30][31][32][33][34][35][36] and acetaminophen. [37][38][39][40][41][42][43][44] Over the past 30 years, acetaminophen overdose has become the most common cause of FHF in the United Kingdom.…”
Section: Chemical Modelsmentioning
confidence: 99%
“…A further model by Kalpana et al 30 examined the issue of toxicity in the context of D-galactosamine and halothane. As listed in Table 2, the outcomes in their experiment were largely similar except for hypoglycemia, which was present.…”
Few conditions in medicine are more dramatic or more devastating than acute liver failure. Our understanding and treatment of this condition have been limited by the lack of satisfactory animal models. The most widely used models consist of surgical anhepatic and devascularization procedures and hepatotoxins, such as galactosamine and acetaminophen. Potential disadvantages with surgical models are their inability to recreate the inflammatory milieu that exists in acute liver failure and their reliance on surgical expertise. Models using hepatotoxins are free of such constraints. Galactosamine-induced hepatotoxicity is more predictable than acetaminophen, but its cost and lack of a human equivalent clinical syndrome has restricted its use. Acetaminophen-based models offer the greatest potential but have proven the most difficult to develop because of difficulties with reproducibility and refractory anemia. Although progress has been made, research must continue in this area to establish an animal model with minimal disadvantages that would accurately reflect the clinical syndrome seen in humans.
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