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Magnetic resonance imaging with hepatospecific contrast agents in cirrhotic rat livers.

Authors: Planchamp, Corinne  Montet, Xavier  Frossard, Jean-Louis  Quadri, Rafael  Stieger, Bruno  Meier, Peter J  Ivancevic, Marko K  Vallée, Jean-Paul  Terrier, François  Pastor, Catherine M 
Citation: Planchamp C, etal., Invest Radiol. 2005 Apr;40(4):187-94.
Pubmed: (View Article at PubMed) PMID:15770136


OBJECTIVE: During biliary cirrhosis in rats, organic anion-transporting peptides (Oatps) and ATP-dependent multidrug resistance-associated protein 2 (Mrp2) that are likely to transport the contrast agent Gd-BOPTA through hepatocytes are down-regulated. However, the consequences of such down-regulation on the signal intensity (SI) enhancement are unknown. Consequently, the aim of our study was to measure the hepatic SI enhancement during Gd-BOPTA perfusion as well as the Oatp and Mrp2 expression in normal and cirrhotic livers.
MATERIALS AND METHODS: The hepatic SI enhancement during Gd-BOPTA perfusion was measured in livers isolated from normal rats and rats that had a bile duct ligation (BDL) 15, 30, and 60 days before the perfusion. Hepatic injury and transporter expression were measured in control and cirrhotic rats.
RESULTS: BDL induced a severe hepatic injury that increased over time with a down-regulation of the transporter expression. The extracellular space (assessed by Gd-DTPA perfusion) increased with the severity of the disease. Gd-BOPTA-induced SI enhancement remained similar in BDL-15 and BDL-30 rats than in control rats but significantly decreased in severe cirrhosis (BDL-60 rats). In comparison, the Mn-DPDP-induced SI enhancement decreases proportionally to the severity of the disease.
CONCLUSION: During biliary cirrhosis, Gd-BOPTA-induced SI enhancement could not be related to the hepatic expression of transporters.

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RGD Object Information
RGD ID: 14700810
Created: 2019-08-20
Species: All species
Last Modified: 2019-08-20
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.