Published in:
01-06-2013 | Research Article
Delayed hepatic signal recovery on ferucarbotran-enhanced magnetic resonance images: an experimental study in rat livers with gadolinium chloride-induced Kupffer cell damage
Authors:
Toshihiro Furuta, Masayuki Yamaguchi, Ryutaro Nakagami, Masaaki Akahane, Manabu Minami, Kuni Ohtomo, Noriyuki Moriyama, Hirofumi Fujii
Published in:
Magnetic Resonance Materials in Physics, Biology and Medicine
|
Issue 3/2013
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Abstract
Objective
Hepatic signal recovery, rather than reduction, in ferucarbotran-enhanced magnetic resonance imaging (MRI) is a potential diagnostic marker of liver damage. We investigated hepatic signal recovery in rats with gadolinium chloride (GdCl3)-induced Kupffer cell (KC) damage.
Materials and methods
Twelve rats received 8 μmol iron/kg of ferucarbotran 1 day after 0–7.5 mg/kg GdCl3 injection (experiment A). Another 12 rats received ferucarbotran followed by GdCl3 injection 6 h later (experiment B). In each experiment, three rats without GdCl3 (“no injury group”) served as control. Another six rats received GdCl3 alone without ferucarbotran. Hepatic signals were assessed on T
2
*
-weighted images for up to 29 days. Iron deposits were histologically examined on day 29.
Results
Hepatic signal recovery was delayed in a GdCl3 dose-dependent manner in experiment A. Gadolinium chloride alone reduced hepatic signal 15 % during this experiment. Hepatic signal recovery was delayed only in rats that received 7.5 mg/kg GdCl3 in experiment B. Hepatic signals negatively correlated with iron deposits in KCs and hepatocytes.
Conclusion
Hepatic signal recovery on ferucarbotran-enhanced MRI was delayed in the context of GdCl3-induced KC damage due to increased hepatic iron deposits. Hepatic signal recovery may be used as a clinical marker of KC damage in liver disorders, including radiation-induced hepatitis.