Magnetic Resonance Imaging of Infarcted Liver Induced by Selective Ligation of Right Portal Vein in Rabbits.
10.3348/jkrs.1994.31.1.99
- Author:
Won Jae LEE
;
Byung Ihn CHOI
;
Jin Wook CHUNG
;
Jae Hyung PARK
;
Joon Koo HAN
;
Jin Mo GOO
;
Man Chung HAN
;
Kyung Mo YEON
;
In Kyu YU
;
Chu Wan KIM
;
Sung Wook CHOO
;
Dae Young YOON
- Publication Type:Original Article
- MeSH:
Cicatrix;
Diagnosis, Differential;
Estrogens, Conjugated (USP);
Giant Cells;
Hemorrhage;
Hemosiderin;
Infarction;
Ligation*;
Liver*;
Magnetic Resonance Imaging*;
Methemoglobin;
Monocytes;
Necrosis;
Portal Vein*;
Protons;
Rabbits*
- From:Journal of the Korean Radiological Society
1994;31(1):99-108
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE:To investigate the changes of abnormal signal intensity of liver infarction in scheduled intervals after ligation of portal vein in rabbit livers with histopathologic correlation. MATERIALS AND METHODS:Liver infarction were induced by selective ligation of the posterior branch of right portal vein in 12 rabbits. T1- and T2-weighted MRI at 2.0T with spin-echo techniques as well as contrastenhanced Tl-weighted MRI with Gd-DTPA(0.1 mmol/kg) were performed 3 hours, 6 hours, 1 day, 3 days, 1 week, and 2 weeks after ligation using two rabbits at each interval. Histopathologic specimens were prepared from six removed livers for comparing the MR findings with the histopathologic findings. The other six rabbits were sectioned transversely in frozen state for comparing MR findings with the macroscopic findings of pathologic areas of the liver. RESULTS: The signal intensity of pathologic hepatic segment showed more hyperintense signal than that of normal segments of the liver on TI-, proton density-, and T2-weighted MR images at every interval after ligation, except both T2WI of 3 hours interval and one T1WI of 2 weeks interval. Main histopathologic findings 3 hours, 6 hours, 1 day, 3 days, and 1 week after ligation were congestion, hemorrhage with necrosis, coagulation necrosis, complete necrosis, and necrosis with scar tissues, respectively. Microscopic specimens with Prussian blue stain 6 hours, and 1 week after ligation showed bluish hue indicating the existence of methemoglobin, and blue particles in giant cells and monocytes indicating engulfing hemosiderin, respectively. CONCLUSION: Changes of the signal intensities on sequential MR images of acutely induced hemorrhagic liver infarction might be due to the rapid oxidative denaturation of hemoglobin in hemorrhages and high signal intensity on Tl-weighted images from the hyperacute stage of a hemorrhagic liver infarction could be due to methemoglobin. Therefore, acutely induced hemorrhagic liver infarction should be included in the differential diagnoses of the hyperintense liver lesions on Tl-weighted images.
