Abstract

BackgroundTo assess the feasibility of noninvasive and quantitative evaluation of hepatic pathophysiological changes in rabbit hepatic warm ischemia-reperfusion injury (WIRI) models by using intravoxel incoherent motion (IVIM), diffusion tensor imaging (DTI) and blood oxygen level dependent (BOLD) MRI.MethodsTwenty rabbits were randomly divided into hepatic WIRI model group and sham-operation group (n = 10 for each group). Hepatic WIRI was induced in rabbit by occluding hepatic inflow for 30 min and reperfusion for 6 h. The control group only underwent laparotomy and liver ligament dissection. IVIM with 11 b values (0 to 800 s/mm2), DTI with 2 b values (0 and 500 s/mm2) on 12 diffusion directions, and BOLD MRI with 9 TE (2.57 to 24.25 ms) were performed at 3 T clinical MR scanner. Rabbits were sacrificed for biochemical and histopathological analysis after MR scanning. All of functional MR, biochemical and histopathological parameters were analyzed by independent sample t test, Mann-Whitney U test, Pearson and Spearman correlation methods.ResultsAll of MR parameters showed moderate to excellent interobserver reproducibility. True diffusion (Dslow), pseudodiffusion (Dfast), perfusion fraction (PF), and mean diffusitivity (MD) were lower in WIRI models than in control rabbits (P < 0.01), R2* was higher in WIRI models than in control rabbits (P < 0.001), while fractional anisotropy (FA) showed no statistical difference. There were significant differences in I score and all of biochemical parameters between the two groups (P < 0.01). Functional MR parameters corresponded well with all of biochemical parameters and some of histopathological parameters (P < 0.05). Histopathological analysis showed the structure and morphology of hepatic lobule was normal and clear in control rabbits, while diffuse hepatocyte swelling, central vein and sinusoids congestion, and inflammatory cell infiltration in WIRI models.ConclusionsIVIM, DTI, and BOLD MRI are noninvasive and useful techniques for assessing the microenvironment changes of hepatic WIRI in rabbit models.

Highlights

  • To assess the feasibility of noninvasive and quantitative evaluation of hepatic pathophysiological changes in rabbit hepatic warm ischemia-reperfusion injury (WIRI) models by using intravoxel incoherent motion (IVIM), diffusion tensor imaging (DTI) and blood oxygen level dependent (BOLD) MRI

  • Twenty adult New Zealand White rabbits weighing 2.53.0 kg were randomly divided into two groups: hepatic WIRI model group (n = 10) and sham-operation control group (n = 10)

  • Comparison of functional MR parameters between two groups True diffusion or pure molecular diffusion (Dslow), Pseudodiffusion or perfusion related diffusion (Dfast), perfusion fraction (PF), and mean diffusitivity (MD) of model group were significantly lower than control group (P < 0.01), while R2* of model group was significantly higher than control group (P < 0.001)

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Summary

Introduction

To assess the feasibility of noninvasive and quantitative evaluation of hepatic pathophysiological changes in rabbit hepatic warm ischemia-reperfusion injury (WIRI) models by using intravoxel incoherent motion (IVIM), diffusion tensor imaging (DTI) and blood oxygen level dependent (BOLD) MRI. Hepatic ischemia–reperfusion injury (IRI) is the most common cause of liver damage during liver transplantation [1]. The hepatic IRI of DCD liver grafts is attributed to blood supply returns to the tissue after a period of ischemia during graft harvest ( called warm ischemia), graft storage (cold ischemia) and graft implantation (reperfusion). Reperfusion of ischemic tissue is essential for survival, it initiates oxidative damage, cell death and aberrant immune responses through the generation of mitochondrial reactive oxygen species (ROS) [10]. Hepatic warm ischemia–reperfusion injury (WIRI) causes sever ischemia and anoxia, oxidation/antioxidation imbalance, and excessive inflammatory response [11], which result in liver microcirculatory disorders and histological damage

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