ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2007
Partial portal vein ligation plus thioacetamide: a method to obtain a new model of cirrhosis and chronic portal hypertension in the rat.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 19 citations in OpenAlex.
- The efficacy of nardostachys jatamansi against the radiation induced haematological damage in rats.Journal of clinical and diagnostic research : JCDR · 2013Article
- Mapping metabolic brain activity in three models of hepatic encephalopathy.International journal of hypertension · 2013Article
- A new phosphorimetry for the determination of trace alkaline phosphatase using multi-wall carbon nanotubes and its diagnosis of human diseases.Journal of fluorescence · 2010Article
- Inflammation: a way to understanding the evolution of portal hypertension.Theoretical biology & medical modelling · 2007Review
- The mast cell integrates the splanchnic and systemic inflammatory response in portal hypertension.Journal of translational medicine · 2007Review
- Constriction rate variation produced by partial ligation of the portal vein at pre-hepatic portal hypertension induced in rats.Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgeryArticle
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
To obtain a new model of chronic portal hypertension in the rat, two classical methods to produce portal hypertension, partial portal vein ligation and the oral administration of thioacetamide (TAA), have been combined. Male Wistar rats were divided into four groups: 1 (control; n = 10), 2 [triple partial portal vein ligation (TPVL); n = 9], 3 (TAA; n = 11), and 4 (TPVL plus TAA; n = 9). After 3 months, portal pressure, types of portosystemic collateral circulation, laboratory hepatic function tests (aspartate aminotransferase, alanine aminotransferase, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase) and liver histology were studied. The animals belonging to group 2 (TPVL) developed extrahepatic portosystemic collateral circulation, associated with mesenteric venous vasculopathy without hepatic destructurization or portal hypertension. Animals from group 3 (TAA) developed cirrhosis and portal hypertension but not extrahepatic portosystemic collateral circulation, or mesenteric venous vasculopathy. Finally, the animals from group 4 (TPVL + TAA) developed cirrhosis, portal hypertension, portosystemic collateral circulation, and mesenteric venous vasculopathy. The association of TPVL and TAA can be used to obtain a model of chronic portal hypertension in the rat that includes all the alterations that patients with hepatic cirrhosis usually have. This could, therefore, prove to be a useful tool to study the pathophysiological mechanisms involved in these alterations.
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