Yin Wu1, Jianan Ren2, Bo Zhou1, Chao Ding1, Jun Chen1, Gefei Wang1, Guosheng Gu1, Song Liu1, Jieshou Li1. 1. Department of Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, PR China. 2. Department of Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, PR China. Electronic address: JiananR@gmail.com.
Abstract
BACKGROUND: Sepsis is a fatal systemic inflammatory response syndrome caused by severe infection. The aim of this study was to measure hepatic microcirculation during the sepsis with laser speckle contrast imaging (LSCI), as well as investigating the underlying mechanisms. METHODS: Sepsis was induced by cecal ligation and puncture. Rats were divided into the sham group and sepsis group. The hepatic microcirculation was monitored with LSCI. In addition, hepatic endothelial function (expression of cell adhesion molecules, coagulation and vascular permeability) and neutrophils accumulation in the liver were compared between the two groups. RESULTS: During the sepsis, hepatic microcirculation decreased dramatically (290.3±70.1 LSPU (laser speckle perfusion units) at baseline vs. 230.4±60.7 LSPU at 12h vs. 125.2±25.4 LSPU at 48h, P<0.001). The rats developed hyperbilirubinemia since 6h. In the early phase of sepsis, the accumulation of neutrophils and formation of microthrombus increased rapidly. In the late phase, hepatic neutrophils accumulation was already at its maximum level. Meanwhile, the endothelial coagulation status shifted from procoagulation to anticoagulation. The vascular leakage was involved in the microcirculation dysfunction since 12h after sepsis. CONCLUSIONS: Hepatic microcirculation dysfunction occurs early during the sepsis and is associated with liver injury. This microcirculation dysfunction is due to neutrophil-endothelium interactions, microthrombus formation and vascular leakage.
BACKGROUND:Sepsis is a fatal systemic inflammatory response syndrome caused by severe infection. The aim of this study was to measure hepatic microcirculation during the sepsis with laser speckle contrast imaging (LSCI), as well as investigating the underlying mechanisms. METHODS:Sepsis was induced by cecal ligation and puncture. Rats were divided into the sham group and sepsis group. The hepatic microcirculation was monitored with LSCI. In addition, hepatic endothelial function (expression of cell adhesion molecules, coagulation and vascular permeability) and neutrophils accumulation in the liver were compared between the two groups. RESULTS: During the sepsis, hepatic microcirculation decreased dramatically (290.3±70.1 LSPU (laser speckle perfusion units) at baseline vs. 230.4±60.7 LSPU at 12h vs. 125.2±25.4 LSPU at 48h, P<0.001). The rats developed hyperbilirubinemia since 6h. In the early phase of sepsis, the accumulation of neutrophils and formation of microthrombus increased rapidly. In the late phase, hepatic neutrophils accumulation was already at its maximum level. Meanwhile, the endothelial coagulation status shifted from procoagulation to anticoagulation. The vascular leakage was involved in the microcirculation dysfunction since 12h after sepsis. CONCLUSIONS:Hepatic microcirculation dysfunction occurs early during the sepsis and is associated with liver injury. This microcirculation dysfunction is due to neutrophil-endothelium interactions, microthrombus formation and vascular leakage.