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1 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA
2 Division of Space Life Sciences, NASA JSC, Universities Space Research Association, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: brd{at}virginia.edu.
The glycocalyx (Gcx) is a complex and poorly understood structure covering the luminal surface of endothelial cells. It is known to be a determinant of vascular rheology and permeability, and may be a key site control site for the vascular injuries caused by ischemia/reperfusion. We used intravital-microscopy to evaluate the effects of ischemia/reperfusion injury (I/R-I) on two properties of Gcx in mouse cremasteric microvessels: exclusion of macromolecules (anionic-dextrans) and intracapillary distribution of red blood cells (RBC). In this model, the Gcx is rapidly modified by I/R-I, with an increase in 70 kDa anionic-dextran-penetration, without measurable effect on the penetration of 580 kDa anionic-dextran or on RBC-exclusion. The effects of I/R-I appear to be mediated by the rapid production of reactive-oxygen species (ROS), because they are ameliorated by the addition of exogenous SOD/Catalase. Intravenous application of allopurinol or heparin also inhibited the effects of I/R-I, and we interpret efficacy of allopurinol as evidence for a role for xanthine-oxidoreductase (XOR) in the response to I/R-I. Heparin, which is hypothesized to displace XOR from a heparin-binding domain in the Gcx, reduced the effects of I/R. The effects of I/R-I were also partially prevented or fully reversed by the intravascular infusion of exogenous hyaluronan. These data demonstrate: 1. The liability of Gcx during I/R-I, 2. The importance of locally produced ROS in the injury to Gcx, and 3. The potential importance of heparin-binding sites in modulating the ROS production. Our findings further highlight the relations between glycosaminoglycans and the pathophysiology of Gcx in vivo.
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