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活体大鼠肝外胆管梗阻后胆汁反流的初始部位

Initial site of bile regurgitation following extrahepatic biliary obstruction in living rats.

作者信息

Watanabe Norihito, Kojima Sei-ichiro, Takashimizu Shinji, Nishizaki Yasuhiro, Kagawa Tatehiro, Phillips M James

机构信息

Division of Gastroenterology, Department of Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

出版信息

J Gastroenterol Hepatol. 2007 Nov;22(11):1983-92. doi: 10.1111/j.1440-1746.2006.04623.x.

Abstract

BACKGROUND AND AIM

The precise mechanism of bile regurgitation from the biliary system to the blood stream still remains to be elucidated. The aim of this study was to examine the initial site of bile regurgitation in vivo after common bile duct (CBD) obstruction by digitally enhanced fluorescence microscopy.

METHODS

The fluorescence excreted into bile canaliculi after the administration of sodium fluorescein was continuously observed in CBD obstruction, using video-enhanced contrast (VEC) microscopy equipped with a silicon intensified target (SIT) camera. The liver histology and the localization of Mg(2+)-ATPase were examined by light and electron microscopy.

RESULTS

By the continuous recording of canalicular fluorescence, the sequential regurgitation of the fluorescence from the canaliculi to the hepatocyte cytoplasm to the sinusoids was distinctively recognized after CBD obstruction. Bile canalicular fluorescence was enhanced, and then the fluorescence of the hepatocyte cytoplasm increased in intensity, followed by regurgitation of the fluorescence to the sinusoids. These in vivo sequences closely correlated with changes in CBD pressure. In zone 1, canalicular fluorescence focally burst into hepatocyte cytoplasm, thus resulting in the formation of fluorescent cells. By light and electron microscopy, the fluorescent cells were found to correspond to the liver cell injury. The reaction products of Mg(2+)-ATPase were incorporated into vesicles with a decreased canalicular activity, and then were transported to the sinusoidal surface after CBD obstruction.

CONCLUSIONS

The initial site of bile regurgitation may be transcellular, and partly involves liver cell injury in zone 1 in extrahepatic biliary obstruction, associated with increased pressure of the biliary system.

摘要

背景与目的

胆汁从胆道系统反流至血流的确切机制仍有待阐明。本研究旨在通过数字增强荧光显微镜检查胆总管(CBD)梗阻后体内胆汁反流的起始部位。

方法

使用配备硅增强靶(SIT)相机的视频增强对比度(VEC)显微镜,连续观察胆总管梗阻后给予荧光素钠后排入胆小管的荧光。通过光镜和电镜检查肝脏组织学及镁离子 -ATP酶的定位。

结果

通过连续记录胆小管荧光,在胆总管梗阻后可清晰观察到荧光从胆小管依次反流至肝细胞胞质再至肝血窦。胆小管荧光增强,随后肝细胞胞质荧光强度增加,接着荧光反流至肝血窦。这些体内过程与胆总管压力变化密切相关。在1区,胆小管荧光局部突然进入肝细胞胞质,从而形成荧光细胞。通过光镜和电镜发现,荧光细胞与肝细胞损伤相对应。胆总管梗阻后,镁离子 -ATP酶的反应产物被并入小管活性降低的小泡中,然后被转运至肝血窦表面。

结论

胆汁反流的起始部位可能是跨细胞的,部分涉及肝外胆管梗阻时1区的肝细胞损伤,且与胆道系统压力升高有关。

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