2019
DOI: 10.1002/jmri.27022
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Multiparametric MRI Evaluation of Liposomal Prostaglandins E1 Intervention on Hepatic Warm Ischemia‐Reperfusion Injury in Rabbits

Abstract: BackgroundLiposomal prostaglandin E1 (Lipo‐PGE1) treatment should protect against hepatic warm ischemia‐reperfusion injury (WIRI). Improved methods are needed for the noninvasive evaluation of hepatic responses to prophylactic Lipo‐PGE1 pretreatment approaches.PurposeTo demonstrate that multiparametric MRI measurements permit noninvasive differentiation of Lipo‐PGE1 treatment outcomes in a hepatic WIRI animal model.Study TypeAnimal study.Animal ModelSeventy rabbits were randomly divided into a sham‐operated gr… Show more

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Cited by 8 publications
(5 citation statements)
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“…IIR might cause a release of inflammatory cytokines, leukocytes, and chemokines, which can lead to “sodium pump” inactivation for the net gain of water in the hepatocytes 20,21 . In accordance with a previous study 22 that showed that the values of f and D * reduced with the aggravation of hepatic injury, this study also showed that the values f and D * gradually decreased from the Sham group to the IR4h group, which indicated that these findings demonstrate a decreased blood volume and the presence of microcirculatory disorder in the liver. The H&E examinations showed that both hepatic sinusoid congestion blocking intrahepatic vessels and hepatocyte edema degeneration compressing intrahepatic vessels caused the changes in f and D * 3,23 …”
Section: Discussionsupporting
confidence: 92%
“…IIR might cause a release of inflammatory cytokines, leukocytes, and chemokines, which can lead to “sodium pump” inactivation for the net gain of water in the hepatocytes 20,21 . In accordance with a previous study 22 that showed that the values of f and D * reduced with the aggravation of hepatic injury, this study also showed that the values f and D * gradually decreased from the Sham group to the IR4h group, which indicated that these findings demonstrate a decreased blood volume and the presence of microcirculatory disorder in the liver. The H&E examinations showed that both hepatic sinusoid congestion blocking intrahepatic vessels and hepatocyte edema degeneration compressing intrahepatic vessels caused the changes in f and D * 3,23 …”
Section: Discussionsupporting
confidence: 92%
“…Even still, several MRI models (such as blood oxygen level-dependent (BOLD) imaging, diffusion tensor imaging (DTI), or T 2 mapping) were used to detect the oxygenation state, water diffusion, or water relaxation time during hepatic I/R injury, respectively. However, those MRI models without contrast agent still suffered from the low sensitivity and specificity for measuring hepatic I/R injury. Thus, for real-time monitoring of the dynamics of redox status during liver I/R injury, MRI probe should be tailored to the reversible, sensitive, dynamic response toward redox homeostasis.…”
Section: Discussionmentioning
confidence: 99%
“…e L2-L3 angles of the experimental group were evidently larger than those of the control group, while the L3-L4, L4-L5, and L5-S1 angles were not (P < 0.05). Li et al [18] ever pointed out that the change of angles in the experimental group resulted from long-term lordosis of lumbar spines, thus paraspinal muscle showing high tension. Longstanding tension would cause lumbar strain, which even reflected to back or legs.…”
Section: Discussionmentioning
confidence: 99%