Repairing the impaired gut vascular barrier as a novel therapeutic target for prolonged postoperative ileus: A scoping review

Abstract

Prolonged postoperative ileus (PPOI) is a common post-surgery iatrogenic complication, with an incidence rate of 10%-28%. Severe PPOI delays postoperative recovery, prolongs hospital stay, and further increases healthcare costs. The pathogenesis of PPOI is extremely complex. The persistent and excessive immune-inflammatory response is currently considered to be the main pathological mechanism of PPOI. Gut vascular barrier (GVB) damage and the resulting vascular inflammatory response are two key factors responsible for sustaining persistent intestinal inflammation in PPOI. This article comprehensively reviews the effects of intestinal microvascular endothelial cell (IMVEC) dysfunction, increased GVB permeability, pathological angiogenesis, and intestinal microvascular hemodynamic alterations on PPOI. Our review indicates that these GVB-related mechanisms collectively exacerbate intestinal inflammation and dysmotility, contributing to the persistence of PPOI. It also discusses the potential of improving IMVEC function, reducing GVB permeability, inhibiting pathological angiogenesis, and ameliorating intestinal microcirculation for preventing and treating PPOI. In conclusion, targeting GVB dysfunction and associated vascular pathology represents a promising therapeutic strategy. Thus, we propose that restoring the impaired GVB may serve as a potential target for therapeutic intervention in PPOI.

Keywords: Gut vascular barrier; Prolonged postoperative ileus; Intestinal microvascular endothelial cells; Therapeutic target; Vascular immunity

Core Tip: Prolonged postoperative ileus (PPOI) is a common iatrogenic complication following surgery, with an incidence rate ranging from 10% to 28%. Damage to the gut vascular barrier (GVB) and the subsequent vascular inflammatory response are key factors that contribute to the persistence of intestinal inflammation in PPOI. This review comprehensively examines the impact of intestinal microvascular endothelial cell dysfunction, increased GVB permeability, pathological angiogenesis, and alterations in intestinal microvascular hemodynamics on PPOI. It suggests that restoring the impaired GVB may present a promising therapeutic target for managing PPOI.