• Investigative Magnetic Resonance Imaging
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• v.7 no.2
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• pp.116-123
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• 2003

Purpose : The present study was undertaken to evaluate the usefulness of cerebral diffusion (DWI) and perfusion MR imaging (PWI) in rabbit models with hyperacute cerebral ischemic infarction. Materials and Methods : Experimental cerebral infarction were induced by direct injection of mixture of Histoacryl glue, lipiodol, and tungsten powder into the internal cerebral artery of 6 New-Zealand white rabbits, and they underwent conventional T1 and T2 weighted MR imaging, DWI, and PWI within 1 hour after the occlusion of internal cerebral artery. The PWI scan for each rabbit was obtained at the level of lateral ventricle and 1cm cranial to the basal ganglia. By postprocessing using special imaging software, perfusion images including cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT) maps were obtained. The detection of infarcted lesion were evaluated on both perfusion maps and DWI. MTT difference time were measured in the perfusion defect lesion and symmetric contralateral normal cerebral hemisphere. Results : In all rabbits, there was no abnormal signal intensity on T2WI. But on DWI, abnormal high signal intensity, suggesting cerebral infarction, were detected in all rabbits. PWI (rCBV, CBF and MTT map) also showed perfusion defect in all rabbits. In four rabbits, the calculated square of perfusion defect in MTT map is larger than that of CBF map and in two rabbits, the calculated size of perfusion defect in MTT map and CBF map is same. Any rabbits do not show larger perfusion defect on CBF map than MTT map. In comparison between CBF map and DWI, 3 rabbits show larger square of lesion on CBF map than on DWI. The others shows same square of lesion on both technique. The size of lesion shown in 6 MTT map were larger than DWI. In three cases, the size of lesion shown in CBF map is equal to DWI. But these were smaller than MTT map. The calculated square of lesion in CBF map, equal to that of DWI and smaller than MTT map was three. And in one case, the calculated square of perfusion defect in MTT map was largest, and that of DWI was smallest. Conclusion : DWI and PWI may be useful in diagnosing hyperacute cerebral ischemic infarction and in e-valuating the cerebral hemodynamics in the rabbits.

• The Korean Journal of Nuclear Medicine
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• v.39 no.3
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• pp.200-208
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• 2005

Purpose: Tc-99m labeled diethylenetriaminepentaacctic acid (DTPA)-coupled galactosylated human serum albumin (GSA) is a currently used imaging agent for asialoglycoprotein receptor (ASGPR) of the liver, but, it has several shortcomings. Recently a new ASGPR imaging agent, $^{99m}Tc$-lactosylated human serum albumin (LSA), with simple labeling procedure, high labeling efficiency, high stability was developed. In order to assess the feasibility of the $^{99m}Tc$-LSA as a ASGPR imaging radiopharmaceuticals, we performed biodistribution study of the tracer in liver injured mice model and the results were compared with histolgic data. Materals and Methods: To induce hepatic damage in ICR mice, diethylnitrosamine (DEN) ($60mg/kg/week{\times}5time$, low dose or $180mg/kg/week{\times}2times$, high dose) and thioacetamide (TAA) ($50mg/kg{\times}1time$) were administrated intraperitoneally. Degree of liver damage was evaluated by tissue hematoxilin-eosin stain, and expression of asialoglycoprotein receptor (ASGPR) was assessed by immunohistochemistry using ASGPR antibody. $^{99m}Tc$-LSA was intravenously administrated via tail vein in DEN or TAA treated mice, and biodistribution study of the tracer was also performed. Results: DEN treated mice showed ballooning of hepatocyte and inflammatory cell infiltration in low dose group and severe hapatocyte necrosis in high dose group, and low dose group showed higher ASGPR staining than control mice in immunohistochemical staining. TAA treated mice showed severe hepatic necrosis. $^{99m}Tc$-LSA Biodistribution study showed that mice with hepatic necrosis induced by high dose DEN or TAA revealed higher blood activity and lower liver activity than control mice, due to slow clearance of the tracer by the liver. The degree of liver uptake was inversely correlated with the degree of histologic liver damage. But low dose DEN treated mice with mild hepatic injury showed normal blood clearance and hepatic activity, partly due to overexpression of ASGPR in mice with mild degree hepatic injury. Conclusion: Liver uptake of $^{99m}Tc$-LSA was inversely correlated with degree of histologic hepatic injury in DEN and TAA treated mice. These results support that $^{99m}Tc$-LSA can be used to evaluate the liver status in liver disease patients.