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Int. J. Mol. Sci. 2015, 16(6), 12092-12107; doi:10.3390/ijms160612092

Anesthetic Propofol Overdose Causes Vascular Hyperpermeability by Reducing Endothelial Glycocalyx and ATP Production

1
Department of Anesthesiology, Chi Mei Medical Center, Liouying, 201, Taikang, Taikang Village, Liuying District, Tainan 736, Taiwan
2
Department of Medical Laboratory Science and Biotechnology, Chung Hwa University of Medical Technology, 89, Wenhwa 1st Street, Rende District, Tainan 717, Taiwan
3
Department of Microbiology and Immunology, Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 250 Wuxing Street, Taipei 110, Taiwan
4
Department of Pathology, Chi Mei Medical Center, 901 Zhonghua Road, Yongkang District, Tainan 710, Taiwan
5
Department of Surgery, Chi Mei Medical Center, 901 Zhonghua Road, Yongkang District, Tainan 710, Taiwan
6
Department of Anesthesiology, Chi Mei Medical Center, 901 Zhonghua Road, Yongkang District, Tainan 710, Taiwan
7
Department of Anesthesiology, College of Medicine, Taipei Medical University, 250 Wuxing Street, Taipei 110, Taiwan
*
Author to whom correspondence should be addressed.
Academic Editor: Joseph V. Moxon
Received: 3 April 2015 / Accepted: 21 May 2015 / Published: 27 May 2015
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Prolonged treatment with a large dose of propofol may cause diffuse cellular cytotoxicity; however, the detailed underlying mechanism remains unclear, particularly in vascular endothelial cells. Previous studies showed that a propofol overdose induces endothelial injury and vascular barrier dysfunction. Regarding the important role of endothelial glycocalyx on the maintenance of vascular barrier integrity, we therefore hypothesized that a propofol overdose-induced endothelial barrier dysfunction is caused by impaired endothelial glycocalyx. In vivo, we intraperitoneally injected ICR mice with overdosed propofol, and the results showed that a propofol overdose significantly induced systemic vascular hyperpermeability and reduced the expression of endothelial glycocalyx, syndecan-1, syndecan-4, perlecan mRNA and heparan sulfate (HS) in the vessels of multiple organs. In vitro, a propofol overdose reduced the expression of syndecan-1, syndecan-4, perlecan, glypican-1 mRNA and HS and induced significant decreases in the nicotinamide adenine dinucleotide (NAD+)/NADH ratio and ATP concentrations in human microvascular endothelial cells (HMEC-1). Oligomycin treatment also induced significant decreases in the NAD+/NADH ratio, in ATP concentrations and in syndecan-4, perlecan and glypican-1 mRNA expression in HMEC-1 cells. These results demonstrate that a propofol overdose induces a partially ATP-dependent reduction of endothelial glycocalyx expression and consequently leads to vascular hyperpermeability due to the loss of endothelial barrier functions. View Full-Text
Keywords: propofol; mice; endothelial cells; glycocalyx; vascular permeability; ATP propofol; mice; endothelial cells; glycocalyx; vascular permeability; ATP
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Lin, M.-C.; Lin, C.-F.; Li, C.-F.; Sun, D.-P.; Wang, L.-Y.; Hsing, C.-H. Anesthetic Propofol Overdose Causes Vascular Hyperpermeability by Reducing Endothelial Glycocalyx and ATP Production. Int. J. Mol. Sci. 2015, 16, 12092-12107.

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