Fig. 1

Sepsis induces pericyte loss, vascular hyporeactivity and leakage in rats. a Mesenteric microvascular networks from CLP and LPS (10 mg/kg)-induced sepsis at 6, 12 and 24 h were stained for NG-2 (pericyte marker; green), PDGFR-β (pericyte marker; green), and CD31 (VEC marker; red). Pericyte coverage rate of endothelium was quantified by analyzing percentage of CD31⁺ capillaries opposed to NG-2⁺ and PDGFR-β⁺ PCs (n = 8 rats). Scale bars: 100 μm. b TEM observation of ultrastructural changes of pericyte in mesenteric venules at 24 h after CLP and LPS administration (yellow arrowheads indicate pericyte loss and swelling, *indicate erythrocyte diapedesis). Scale bars: 2 μm. c Changes in vascular response of mesenteric arterioles to NE and Ach in vivo (n = 8 rats). d Vascular leakage of mesenteric venules measured by the appearance of intravenously injected FITC–BSA and quantitation of FITC–BSA⁺ vessel (n = 8 rats). Scale bars: 50 μm. e Representative TEM images of tight junctions in mesenteric venules after CLP and LPS administration at 24 h (green arrow indicate the tight junction, red arrowheads indicate the endothelial fragments and disrupted VEC junctions). Scale bars: 1 μm. PC pericyte, CLP cecal ligation and puncture, LPS lipopolysaccharides, NG-2 nerve/glial antigen 2, PDGFR-β platelet-derived growth factor receptor beta, VEC vascular endothelial cell, RBC red blood cell, L lumen, NE norepinephrine, Ach acetylcholine, MA mesenteric arteriole, TJ tight junction, TEM transmission electron microscopy. Data shown as mean ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 vs. Sham (one-way ANOVA)