Yi Liu1, Tao Lu1, Congcong Wang1, Hui Li2, Ke Xu1, Peiling Li1. 1. Department of Radiology, The First Clinical Hospital of China Medical University, Shenyang 110001, China. 2. Department of Radiology, Shengjing Hospital of China Medical University, Shenyang 110004, China.
Abstract
BACKGROUND: To prospectively evaluate the stepwise changes that occur in intra-nodular microvessels and microcirculation during the carcinogenesis process of hepatocellular nodules by using in vivo fluorescent microscopy, and to compare these with pathological changes. METHODS: Forty-five 10-week-old male Wistar rats received drinking water containing N-nitrosomorpholine at 10 mg/100 mL for 18weeks to develop multiple hepatocellular carcinomas (HCC) and dysplastic nodules (DN) in the liver; meanwhile, the non-lesion liver tissues become fibrotic. The microvascular morphological change and hemodynamic change of two lesion areas (HCC or DN) and one non-lesion area in each rat were observed with in vivo fluorescent microscope. After in vivo microscopy, 90 nodules and 45 non-lesion liver tissues that were observed were removed for pathological study. The microvessel density (MVD), branch density (BD), and cell density (CD) of these lesions were compared with the Kruskal-Wallis test and Mann-Whitney test, with an overall statistical significance of 0.05. RESULTS: The intra-nodular microvessels appeared tortuous, with irregular branching and abrupt diameter changes to form irregular convoluted networks in the HCC. This was distinctly different from the appearance of DN and non-lesion liver parenchyma. The MVD and BD of HCC were less than that of the DN and non-lesion liver parenchyma (P<0.01), and the BD of DN was also less than that of the non-lesion liver parenchyma (P<0.05). However, the MVD of the DN was similar to that of the non-lesion liver parenchyma (P>0.05). The CD of HCC was more than that of the DN and non-lesion liver parenchyma (P<0.05), and the CD of DN was also more than that of the non-lesion liver parenchyma (P<0.05). CONCLUSIONS: Concurrent with the carcinogenesis process of the hepatocellular nodule, both the intra-nodular microvascular morphology and hemodynamics were stepwise changed, and the number of the intravascular lumen of intranodular microvessels decreased due to the infiltration and compression of intra-nodular parenchymal cells.
BACKGROUND: To prospectively evaluate the stepwise changes that occur in intra-nodular microvessels and microcirculation during the carcinogenesis process of hepatocellular nodules by using in vivo fluorescent microscopy, and to compare these with pathological changes. METHODS: Forty-five 10-week-old male Wistar rats received drinking water containing N-nitrosomorpholine at 10 mg/100 mL for 18weeks to develop multiple hepatocellular carcinomas (HCC) and dysplastic nodules (DN) in the liver; meanwhile, the non-lesion liver tissues become fibrotic. The microvascular morphological change and hemodynamic change of two lesion areas (HCC or DN) and one non-lesion area in each rat were observed with in vivo fluorescent microscope. After in vivo microscopy, 90 nodules and 45 non-lesion liver tissues that were observed were removed for pathological study. The microvessel density (MVD), branch density (BD), and cell density (CD) of these lesions were compared with the Kruskal-Wallis test and Mann-Whitney test, with an overall statistical significance of 0.05. RESULTS: The intra-nodular microvessels appeared tortuous, with irregular branching and abrupt diameter changes to form irregular convoluted networks in the HCC. This was distinctly different from the appearance of DN and non-lesion liver parenchyma. The MVD and BD of HCC were less than that of the DN and non-lesion liver parenchyma (P<0.01), and the BD of DN was also less than that of the non-lesion liver parenchyma (P<0.05). However, the MVD of the DN was similar to that of the non-lesion liver parenchyma (P>0.05). The CD of HCC was more than that of the DN and non-lesion liver parenchyma (P<0.05), and the CD of DN was also more than that of the non-lesion liver parenchyma (P<0.05). CONCLUSIONS: Concurrent with the carcinogenesis process of the hepatocellular nodule, both the intra-nodular microvascular morphology and hemodynamics were stepwise changed, and the number of the intravascular lumen of intranodular microvessels decreased due to the infiltration and compression of intra-nodular parenchymal cells.
Entities:
Keywords:
Hepatocellular carcinoma (HCC); angioarchitecture; hepatocellular dysplastic nodules; in vivo fluorescent microscopy; microvessel density (MVD)