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Morphometric changes and imaging findings of diffuse liver disease in relation to intrahepatic hemodynamics.
Japanese Journal of Radiology ( IF 2.9 ) Pub Date : 2020-04-28 , DOI: 10.1007/s11604-020-00978-6
Kumi Ozaki 1 , Kazuto Kozaka 2 , Yasuo Kosaka 2 , Hirohiko Kimura 1 , Toshifumi Gabata 2
Affiliation  

Diffuse hepatic diseases have a variety of etiologies, with each showing characteristic morphometric changes. These changes are closely related to micro- and macro-level intrahepatic hemodynamics, in addition to the specific underlying pathophysiology. Short-term disorders in intrahepatic hemodynamics caused by each pathophysiological condition are compensated for by the balance of blood perfusion systems using potential trans-sinusoidal, transversal, and transplexal routes of communication (micro-hemodynamics), while long-term alterations to the intrahepatic hemodynamics result in an increase in total hepatic vascular resistance. Blood flow disorders induced by this increased vascular resistance elicit hepatic cellular necrosis and fibrosis. These changes should be uniformly widespread throughout the whole liver. However, morphometric changes do not occur uniformly, with shrinkage or enlargement not occurring homogeneously. Against this background, several macro-intrahepatic hemodynamic effects arise, such as asymmetrical and complicating morphometric structures of the liver, intricate anatomy of portal venous flow and hepatic venous drainage, and zonal differentiation between central and peripheral zones. These hemodynamic factors and pathophysiological changes are related to characteristic morphometric changes in a complicated manner, based on the combination of selective atrophy and compensatory hypertrophy (atrophy–hypertrophy complex). These changes can be clearly depicted on CT and MR imaging.

中文翻译:

与肝内血流动力学相关的弥漫性肝病的形态学变化和影像学表现。

弥漫性肝病有多种病因,每种都表现出特征性的形态学变化。除了特定的潜在病理生理学外,这些变化还与微观和宏观水平的肝内血流动力学密切相关。由各种病理生理状况引起的肝内血流动力学的短期障碍通过使用潜在的跨正弦、横向和跨神经传导途径(微血流动力学)的血液灌注系统的平衡得到补偿,而肝内血流动力学的长期改变导致总肝血管阻力增加。这种增加的血管阻力引起的血流障碍引起肝细胞坏死和纤维化。这些变化应该在整个肝脏中均匀分布。然而,形态变化不均匀发生,收缩或扩大不均匀发生。在此背景下,出现了几种宏观肝内血流动力学效应,例如肝脏的不对称和复杂的形态结构、门静脉血流和肝静脉引流的复杂解剖结构,以及中央和外周区域之间的带状分化。基于选择性萎缩和代偿性肥大(萎缩-肥大复合体)的组合,这些血流动力学因素和病理生理变化以复杂的方式与特征性形态学变化相关。这些变化可以在 CT 和 MR 成像上清楚地描绘出来。例如肝脏的不对称和复杂的形态测量结构,门静脉血流和肝静脉引流的复杂解剖结构,以及中央和外围区域之间的带状分化。基于选择性萎缩和代偿性肥大(萎缩-肥大复合体)的组合,这些血流动力学因素和病理生理变化以复杂的方式与特征性形态学变化相关。这些变化可以在 CT 和 MR 成像上清楚地描绘出来。例如肝脏的不对称和复杂的形态测量结构,门静脉血流和肝静脉引流的复杂解剖结构,以及中央和外围区域之间的带状分化。基于选择性萎缩和代偿性肥大(萎缩-肥大复合体)的组合,这些血流动力学因素和病理生理变化以复杂的方式与特征性形态学变化相关。这些变化可以在 CT 和 MR 成像上清楚地描绘出来。基于选择性萎缩和代偿性肥大(萎缩-肥大复合体)的组合。这些变化可以在 CT 和 MR 成像上清楚地描绘出来。基于选择性萎缩和代偿性肥大(萎缩-肥大复合体)的组合。这些变化可以在 CT 和 MR 成像上清楚地描绘出来。
更新日期:2020-04-28
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