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World J Hepatol. Dec 28, 2016; 8(36): 1602-1609
Published online Dec 28, 2016. doi: 10.4254/wjh.v8.i36.1602
Restructuring of the vascular bed in response to hemodynamic disturbances in portal hypertension
Dmitry Victorovich Garbuzenko, Nikolay Olegovich Arefyev, Dmitry Vladimirovich Belov
Dmitry Victorovich Garbuzenko, Nikolay Olegovich Arefyev, Department of Faculty Surgery, South Ural State Medical University, 454092 Chelyabinsk, Russia
Dmitry Vladimirovich Belov, Department of Hospital Surgery, South Ural State Medical University, 454092 Chelyabinsk, Russia
Author contributions: Garbuzenko DV contributed to the conception and design, acquisition, analysis and interpretation of data, drafting the article, final approval of the version; all authors wrote this manuscript.
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dmitry Victorovich Garbuzenko, MD, PhD, Professor, Department of Faculty Surgery, South Ural State Medical University, Box 12317, 454092 Chelyabinsk, Russia. garb@inbox.ru
Telephone: +8-909-7459826 Fax: +8-351-2687772
Received: August 18, 2016
Peer-review started: August 19, 2016
First decision: September 13, 2016
Revised: September 23, 2016
Accepted: November 1, 2016
Article in press: November 2, 2016
Published online: December 28, 2016
Processing time: 130 Days and 11 Hours
Abstract

In recent years, defined progress has been made in understanding the mechanisms of hemodynamic disturbances occurring in liver cirrhosis, which are based on portal hypertension. In addition to pathophysiological disorders related to endothelial dysfunction, it was revealed: There is the restructuring of the vasculature, which includes vascular remodeling and angiogenesis. In spite of the fact that these changes are the compensatory-adaptive response to the deteriorating conditions of blood circulation, taken together, they contribute to the development and progression of portal hypertension causing severe complications such as bleeding from esophageal varices. Disruption of systemic and organ hemodynamics and the formation of portosystemic collaterals in portal hypertension commence with neovascularization and splanchnic vasodilation due to the hypoxia of the small intestine mucosa. In this regard, the goal of comprehensive treatment may be to influence on the chemokines, proinflammatory cytokines, and angiogenic factors (vascular endothelial growth factor, placental growth factor, platelet-derived growth factor and others) that lead to the development of these disorders. This review is to describe the mechanisms of restructuring of the vascular bed in response to hemodynamic disturbances in portal hypertension. Development of pathogenetic methods, which allow correcting portal hypertension, will improve the efficiency of conservative therapy aimed at prevention and treatment of its inherent complications.

Keywords: Portal hypertension; Vascular remodeling; Angiogenesis; Pathogenesis; Liver cirrhosis

Core tip: The purpose of the review is to describe the mechanisms of restructuring of the vascular bed in response to hemodynamic disturbances in portal hypertension. In addition to pathophysiological disorders related to endothelial dysfunction, it was revealed: There is the restructuring of the vasculature, which includes vascular remodeling and angiogenesis. In spite of the fact that these changes are the compensatory-adaptive response to the deteriorating conditions of blood circulation, taken together, they contribute to the development and progression of portal hypertension causing severe complications such as bleeding from esophageal varices.