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中华普通外科学文献(电子版) ›› 2026, Vol. 20 ›› Issue (01) : 10 -17. doi: 10.3877/cma.j.issn.1674-0793.2026.01.003

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门静脉高压症:侧支循环形成和脾大的临床意义与干预策略
董伟, 褚海波()   
  1. 266300 青岛,同济大学附属东方医院胶州医院普通外科
  • 收稿日期:2025-07-22 出版日期:2026-02-01
  • 通信作者: 褚海波

Portal hypertension: clinical significance and intervention strategies of collateral circulation formation and splenomegaly

Wei Dong, Haibo Chu()   

  1. Department of General Surgery, Jiaozhou Branch of Shanghai East Hospital, Tongji University, Jiaozhou 266300, China
  • Received:2025-07-22 Published:2026-02-01
  • Corresponding author: Haibo Chu
引用本文:

董伟, 褚海波. 门静脉高压症:侧支循环形成和脾大的临床意义与干预策略[J/OL]. 中华普通外科学文献(电子版), 2026, 20(01): 10-17.

Wei Dong, Haibo Chu. Portal hypertension: clinical significance and intervention strategies of collateral circulation formation and splenomegaly[J/OL]. Chinese Archives of General Surgery(Electronic Edition), 2026, 20(01): 10-17.

门静脉高压症(PH)是一种门静脉压力病理性升高所致的临床综合征。PH的病理生理特征是肝纤维化,血管阻力增加,门静脉压力升高;侧支循环形成和内脏动脉扩张共同作用,导致门静脉血流量增加。门体分流和细菌移位产生大量血管扩张因子,体循环血容量重新分布,出现有效血容量不足。高动力循环综合征促进食管胃静脉曲张和脾肿大的发展。PH时脾静脉血流受阻,脾窦扩张充血,刺激脾髓样细胞增生及纤维组织沉积,导致脾功能亢进。脾肿大是进展期慢性肝病和PH的重要标志。促血管生成因子通过调控血管新生,在侧支循环建立和脾脏病理性肿大机制中起着重要作用。PH血流动力学异常及相关代偿通路是靶向治疗的关键靶点,但治疗策略的优化仍需解决疗效异质性和长期安全性的争议。本文重点阐述PH侧支循环形成和脾肿大的病理机制与临床意义、合理的治疗方法以及血管重塑的干预措施。

Portal hypertension (PH) is a common clinical syndrome characterized by a pathologic increase in portal venous pressure, its pathophysiological characteristics occurs owing to extensive fibrosis within the liver parenchyma, causing increased vascular resistance and elevated portal pressure. As PH develops, collateral vessel formation and arterial vasodilation progress, enhancing the blood flow to the portal circulation. Increased levels of circulatory vasodilators are believed to be caused by portosystemic shunting and bacterial translocation, leading to the redistribution of the blood volume with central hypovolemia. Hyperdynamic circulatory syndrome promotes the development of esophagogastric varices and splenomegaly. Cirrhosis-induced blood flow obstruction leads to the splenic sinusoidal dilation and congestion, hyperplasia of fibrous tissue, and proliferation of splenic myeloid cells, culminating in hypersplenism. This condition is an important sign of advanced chronic liver disease and PH. Angiogenic factors play a central role in the establishment of collateral circulation and the mechanism of splenic pathological enlargement by regulating angiogenesis. PH hemodynamic abnormalities and associated compensatory pathways represent key targets for targeted therapy. However, the optimization of therapeutic strategies still requires addressing controversies regarding efficacy heterogeneity and long-term safety. This review focuses on our current understanding of the pathophysiological mechanism of collateral circulation and splenomegaly, clinical significance, and novel therapeutic approaches for cirrhosis. Interventions targeting these vascular alterations are expected to exert beneficial effects in managing PH in the future.

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