In Vivo Magnetic Resonance Imaging of Embryonic Neural Grafts in a Rat Model of Striatonigral Degeneration (Multiple System Atrophy)

The cerebroprotective properties of the competitive NMDA antagonist d-( E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116) were evaluated in a rat model of focal cerebral ischemia. CGP 40116 (5–40 mg/kg i.v.) was injected immediately following permanent occlusion of the left middle cerebral artery (MCA). MK 801 (1 or 3 mg/kg i.v.), d-CPPene (20 mg/kg i.v.), and CGS 19755 (40 mg/kg i.v.) were used for comparison. Lesion volume was assessed using in vivo magnetic resonance imaging, which in initial experiments with parallel histological determinations proved to be an accurate method for the measurement of brain infarction and the determination of a cerebroprotective drug effect. CGP 40116 dose-dependently reduced the volume of cortical infarction, with an ED50 of 11 mg/kg i.v. and a maximal effect equivalent to a 62% reduction in cortical edema volume. Its cerebroprotective efficacy was thus comparable to that of MK 801. The rank order of potency for the NMDA antagonists was MK 801 > CGP 40116 ∼ d-CPPene > CGS 19755. Neuroprotection by CGP 40116 was still apparent when treatment was started 30 min after MCA occlusion. It is concluded that CGP 40116 is an effective cerebroprotectant with potential clinical utility for amelioration of focal cerebral ischemic damage.

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Rat model of reperfused partial liver infarction: Characterization with multiparametric magnetic resonance imaging, microangiography, and histomorphology

Acta Radiologica ◽

10.1080/02841850802647021 ◽

2009 ◽

Vol 50 (3) ◽

pp. 276-287 ◽

Cited By ~ 19

Author(s):

X. Wu ◽

H. Wang ◽

F. Chen ◽

L. Jin ◽

J. Li ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Rat Model ◽

Normal Liver ◽

Initial Slope ◽

Dynamic Susceptibility ◽

Resonance Imaging ◽

K Value ◽

Contrast Enhanced

Background: Rat model of reperfused partial liver infarction (RPLI) has been increasingly used in studying new diagnostics and therapeutics. Purpose: To characterize the RPLI model using magnetic resonance imaging (MRI), microangiography, and histopathology. Material and Methods: RPLI was induced in eight rats by occluding hepatic inflow to the right liver lobe for 3 hours. MRI was performed at a 1.5T clinical scanner 6 hours after reperfusion to obtain T2-weighted (T2WI), T1-weighted (T1WI), contrast-enhanced (CE) T1WI, diffusion-weighted imaging (DWI) with apparent diffusion coefficient (ADC) maps, T1-weighted dynamic contrast-enhanced (T1-DC) perfusion-weighted imaging (PWI), and T2*-weighted dynamic susceptibility contrast-enhanced (T2*-DSC) PWI images. Rats were sacrificed for microangiography and histomorphology. In vivo morphological and functional MRI parameters, including maximum initial slope (MIS), K value, relative blood flow (rBF), relative blood volume (rBV), time to peak (TTP), and mean transit time (MTT), were matched with postmortem findings. Results: The infarcted lobe was conspicuous from normal liver with lower and higher signal intensity on T1WI ( P=0.018) and T2WI ( P=0.001), respectively. Contrast between infarcted and normal liver reversed on CE-T1WI after gadolinium injection. The infarction averaged 37.5% of total liver volume. DWI and ADC maps were able to detect subtle perfusion-related differences ( P<0.05). With T1-DC-PWI, increased extravasation and vascular permeability were reflected by significantly greater MIS ( P=0.034) and K value ( P=0.014) in infarction. T2*-DSC-PWI showed lower rBF and rBV with shorter TTP and MTT in infarcted liver ( P<0.05). In vivo MRI findings corresponded well with postmortem outcomes. Conclusion: RPLI in rats could be characterized by multiparametric MRI and postmortem assessments, with insight into the no-reflow phenomenon, which implies its further application for preclinical assessments of new pharmaceutics.

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