首页> 外文期刊>American Journal of Physiology >Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow.
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Hepatic neovascularization after partial portal vein ligation: novel mechanism of chronic regulation of blood flow.

机译:结扎部分门静脉后的肝新血管形成:慢性调节血流的新机制。

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摘要

The present study was undertaken to investigate hepatic microcirculatory response following partial portal vein ligation (PPVL) in rats. Portal pressure was markedly increased 2-6 wk after PPVL, but no significant reduction in sinusoidal perfusion and hepatocellular injury were detected. However, marked neovascularization was observed in PPVL rats using intravital microscopy and scanning electron microscopy (SEM). Extremely high red blood cell velocity (2,000-4,900 microm/s) was seen in these vessels. Injection of fluorescein sodium via the carotid artery revealed that the neovessels originated from the hepatic arterial vasculature. This was further confirmed by clamping the common hepatic artery and phenylephrine injection from the carotid artery. These vessels maintained sufficient flow after massive sinusoidal shutdown elicited by the portal infusion of endothelin receptor B agonist IRL-1620. SEM also showed extensive neovascularization at the hilum. Additionally, clamping the portal vein decreased sinusoidal perfusion only by 9.5% in PPVL, whereas a 71.2% decrease was observed in sham. These results strongly suggest that the liver maintains its microcirculatory flow by vascular remodeling from the hepatic arterial vasculature following PPVL.
机译:本研究旨在调查大鼠部分门静脉结扎(PPVL)后的肝微循环反应。 PPVL后2-6周,门静脉压力显着增加,但未检测到正弦曲线灌注和肝细胞损伤的显着降低。然而,使用活体显微镜和扫描电子显微镜(SEM)在PPVL大鼠中观察到明显的新血管形成。在这些血管中观察到极高的红细胞速度(2,000-4,900 microm / s)。通过颈动脉注射荧光素钠显示,新血管起源于肝动脉脉管系统。通过钳夹肝总动脉和从颈动脉注射去氧肾上腺素进一步证实了这一点。在通过内皮素受体B激动剂IRL-1620的门静脉输注引发大量正弦曲线关闭后,这些血管保持足够的流量。扫描电镜还显示了肺门广泛的新血管形成。此外,在PPVL中夹住门静脉可使正弦灌注仅减少9.5%,而在假手术中仅可减少71.2%。这些结果有力地表明,通过PPVL后肝动脉血管系统的血管重塑,肝脏可以维持其微循环血流。

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