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肝动脉灌注对于大鼠自发性恢复肝静脉流出道阻塞至关重要。

Hepatic arterial perfusion is essential for the spontaneous recovery from focal hepatic venous outflow obstruction in rats.

机构信息

Department of General, Visceral and Transplantation Surgery, University Hospital, Essen, Germany.

出版信息

Am J Transplant. 2011 Nov;11(11):2342-52. doi: 10.1111/j.1600-6143.2011.03682.x. Epub 2011 Aug 10.

Abstract

We previously observed that focal hepatic venous outflow obstruction recovered spontaneously by the formation of sinusoidal canals in a rat model of portal hyperperfusion. We aimed to investigate whether the lack of hepatic arterial perfusion aggravates parenchymal damage, decelerates recovery and influences the formation of sinusoidal canals after focal hepatic venous outflow obstruction. Rats were subjected to arterialized versus nonarterialized syngeneic liver transplantation after ligating the right median hepatic vein in the donor. Hepatic damage, microcirculation, regeneration and vascular remodeling were evaluated. In arterialized-recipients, confluent necrosis interspersed with viable periportal islands of hepatocytes, and vascularized sinusoidal canals with visible blood flow, surrounded by normal sinusoidal structure, were visible on postoperative day (POD) 2. Complete parenchymal recovery was consequently established by resorption of necrosis and hepatocyte proliferation, detected in viable portal islands and border zone. Lack of hepatic arterial perfusion caused complete necrosis in the obstruction zone without viable hepatocytes in the periportal area on POD2. Hepatocyte proliferation was only visible in the border zone. On POD28, perfused vascular structures, without neighboring normal sinusoidal structures, were observed in the scar-like area. Hepatic arterial perfusion determined the extent of hepatic necrosis, the formation of vascularized sinusoidal canals and the parenchymal recovery, after focal hepatic venous outflow obstruction.

摘要

我们之前观察到,在门静脉高压症大鼠模型中,肝静脉流出道阻塞通过窦状隙管的形成而自发恢复。我们旨在研究肝动脉灌注缺失是否会加重实质损伤、减缓恢复过程并影响肝静脉流出道阻塞后窦状隙管的形成。在供体中结扎右中肝静脉后,大鼠接受动脉化或非动脉化同种异体肝移植。评估肝损伤、微循环、再生和血管重塑。在动脉化受者中,术后第 2 天可见融合性坏死,其间散在有存活的门脉周围肝细胞岛,以及可见血流的血管化窦状隙管,周围有正常的窦状结构。通过坏死吸收和可见于存活门脉岛和边缘区的肝细胞增殖,随后确立了完全的实质恢复。肝动脉灌注缺失导致阻塞区完全坏死,门脉周围区无存活肝细胞,在术后第 2 天。肝细胞增殖仅见于边缘区。在术后第 28 天,在瘢痕样区域观察到有灌注的血管结构,而无邻近的正常窦状结构。肝动脉灌注决定了肝静脉流出道阻塞后肝坏死的程度、血管化窦状隙管的形成和实质的恢复。

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