Delayed hepatic signal recovery on ferucarbotran-enhanced magnetic resonance images: an experimental study in rat livers with gadolinium chloride-induced Kupffer cell damage

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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.