Abstract
To develop a reliable surgical model of acute hepatic failure and hyperammonemia in rats that avoids porto-systemic shunt and bile duct ligation, applicable to hepatic encephalopathy research. The pedicles of right lateral and caudate lobes were exposed and clamped. One hour later, the animal was reopened, clamps were released and anterior subtotal hepatectomy (resection of median and left lateral lobes) was performed, comprising 75% of liver removal. Four hours after hepatectomy, blood samples and liver tissues were collected from ALF and control groups. Differences between ALF and control groups were significant for ALT, AST, total and direct bilirubin, sodium, potassium, alkaline phosphatasis, gamma-glutamyltransferase and most important, ammonia. Histologically, significant differences were noticed between groups. The model is useful for the study of specific aspects of ALF and the development of new therapeutic approaches.
Highlights
Acute liver failure (ALF) is a morbid condition that may result in severe neurological complications such as hepatic encephalopathy and brain edema leading to intracranial hypertension, brain herniation, and death
Histological liver assessment showed a menagerie of alterations in ALF group (Figure 7)
Results of the present study reveal significant alterations in hepatic enzymes, sodium, potassium, total/direct bilirubin and hyperammonemia resulting from hepatic devascularization followed 75% liver resection
Summary
Acute liver failure (ALF) is a morbid condition that may result in severe neurological complications such as hepatic encephalopathy and brain edema leading to intracranial hypertension, brain herniation, and death. Despite several advances in the clinical management of patients with acute liver failure (ALF), this condition remains extremely serious and results in high mortality rates. The difficulties inherent to the management of patients with ALF can be explained in part by the serious systemic and neurological complications of ALF, which include hypoglycemia, renal failure, coagulopathy, sepsis, multiorgan failure, intracranial hypertension, and hepatic encephalopathy[2]. Liver transplantation remains the only effective treatment of ALF, but its availability is often limited by the chronic shortage of donor livers. That emphasizes the need in developing new strategies for the management and treatment of ALF
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