Division of Gastroenterology, Taipei Veterans General Hospital, Beitou District, Taipei city, Taiwan, Republic of China.
Dig Dis Sci. 2011 Feb;56(2):417-24. doi: 10.1007/s10620-010-1302-6. Epub 2010 Jul 16.
Portal hypertension induced the formation of portal-systemic collaterals. Revealing the developmental change of portal-systemic collaterals is important for future therapy.
We observed the evolution of an accessible shunting vessel, the spleno-renal shunt (SRS), in rats after induction of portal hypertension by partial portal vein ligation (PVL). The hemodynamic and histological assessments of SRS were performed by transit time ultrasound and immunohistochemical studies.
The portal pressure of PVL rats surged to 16.5 ± 1.1 mmHg on day 1 after ligation surgery and was maintained at a significantly higher level (13.0 ± 0.4 mmHg) to day 14 when compared to sham rats (p < 0.05). The size or flow of SRS in PVL rats did not change immediately after portal pressure surge. Instead, they increased rapidly on day 4, peaked on day 7, and stabilized thereafter. The size and flow were greater and the resistance of SRS was lower in PVL rats after day 7 (p < 0.05). The anti-Ki67 immunohistochemical study demonstrated positive staining of endothelium in SRS and negative in portal vein or aorta of PVL rats. In addition, the endothelial cells of SRS were stained positive for CD31 and KLF5.
We concluded that the pressure-induced opening of pre-existing vessels was not the primary underlying mechanism in the formation of SRS. Endothelial proliferating and vascular remodeling process participated actively during the development of SRS. These observations can be used for studying the pathogenesis and developing more effective anti-portal hypertensive therapy in the future.
门静脉高压导致门体侧支循环形成。揭示门体侧支循环的发育变化对于未来的治疗至关重要。
我们观察了大鼠门静脉高压诱导后门体分流血管,脾肾分流(SRS)的演变。通过瞬时超声和免疫组织化学研究对 SRS 的血流动力学和组织学评估。
PVL 大鼠的门静脉压力在结扎手术后第 1 天飙升至 16.5 ± 1.1mmHg,并在第 14 天维持在显著更高的水平(13.0 ± 0.4mmHg),与假手术大鼠相比(p < 0.05)。SRS 的大小或流量在门静脉压力飙升后并未立即发生变化。相反,它们在第 4 天迅速增加,在第 7 天达到峰值,此后稳定下来。第 7 天以后,PVL 大鼠的 SRS 大小和流量更大,阻力更低(p < 0.05)。Ki67 免疫组织化学研究表明,SRS 内皮呈阳性染色,而 PVL 大鼠的门静脉或主动脉呈阴性染色。此外,SRS 的内皮细胞对 CD31 和 KLF5 呈阳性染色。
我们得出结论,压力诱导的预先存在的血管开放不是 SRS 形成的主要潜在机制。内皮增殖和血管重塑过程在 SRS 的发展过程中积极参与。这些观察结果可用于研究发病机制,并在未来开发更有效的抗门静脉高压治疗方法。