Di Pascoli Marco, Sacerdoti David, Pontisso Patrizia, Angeli Paolo, Bolognesi Massimo
Unit of Internal Medicine and Hepatology (UIMH), Department of Medicine - DIMED, University of Padova, Padua, Italy.
J Vasc Res. 2017;54(2):92-99. doi: 10.1159/000462974. Epub 2017 Apr 13.
In liver cirrhosis, portal hypertension is a consequence of enhanced intrahepatic vascular resistance and portal blood flow. Significant vasodilation in the arterial splanchnic district is crucial for an increase in portal flow. In this pathological condition, increased levels of circulating endogenous vasodilators, including nitric oxide, prostacyclin, carbon monoxide, epoxyeicosatrienoic acids, glucagon, endogenous cannabinoids, and adrenomedullin, and a decreased vascular response to vasoconstrictors are the main mechanisms underlying splanchnic vasodilation. In this review, the molecular pathways leading to splanchnic vasodilation will be discussed in detail.
在肝硬化中，门静脉高压是肝内血管阻力增加和门静脉血流的结果。内脏动脉区显著的血管舒张对于门静脉血流增加至关重要。在这种病理状态下，循环中内源性血管舒张剂水平升高，包括一氧化氮、前列环素、一氧化碳、环氧二十碳三烯酸、胰高血糖素、内源性大麻素和肾上腺髓质素，以及血管对血管收缩剂的反应降低，是内脏血管舒张的主要机制。在本综述中，将详细讨论导致内脏血管舒张的分子途径。
