Development of the Damaged Glycocalyx Hypothesis - A Review
A.J. Drake-Holland, M.I.M. Noble*
We have reviewed the literature from 2008 up to 2018 that is relevant to our 2008 postulate that arterial glycocalyx dysfunction is the first step in the atherothombotic process. It would appear from this survey that the hypothesis is still a reasonable one. Vascular glycocalyx dysfunction has been shown to alter fluid exchange with tissue and is involved in oedema and inflammation formation, leading to revised equations for the Starling principle. Interactions between anticoagulant factors bound to the vascular glycocalyx have been postulated to protect vessels from intravascular thombosis. The glycocalyx, according to all authors that we have reviewd, is negatively charged, but we found no measurement of glycocalyx electrical potential. This negativity is suggested as a mechanism for repulsion of adhesion molecules. We suggest that future work should focus on the electrophysiology, e.g., endothelial cells are highly negatively charged as are leukocytes and platelets. We postulate that electrostatic repulsion of like charges may play an important role in the protective function of the vascular glycocalyx, and its failure during dysfunction may contribute to the initiation of arterial disease