Biomarkers of Glycocalyx Injury are Associated with Delayed Cerebral iIchemia following Aneurysmal Subarachnoid Hemorrhage – A Case Series Supporting a New Hypothesis


  1. Bell, J.D.
  2. Rhind, S.G.
  3. Di Battista, A.P.
  4. Macdonald, R.L.
  5. Baker, A.J.
Corporate Authors
Defence Research and Development Canada, Toronto Research Centre , Toronto ON (CAN);University of Toronto, Toronto Ont (CAN) Department of Anesthesia
Background: Delayed cerebral ischemia (DCI) contributes to morbidity following aneurysmal subarachnoid hemorrhage; however, its etiology remains poorly understood. DCI is not only a consequence of angiographic vasospasm, but also involves microthrombosis and neuroinflammation, two events with unexplained phenomenology. The vascular endothelial glycocalyx mediates platelet aggregation and endothelial cell-leukocyte interactions and may play an important role in DCI pathogenesis. Methods: We present a case series in which we conducted multiplex and singlet enzyme-linked immunosorbent assays of endothelial, glycocalyx, inflammatory, and neuroinjury proteins in both CSF and plasma in three patients during active DCI following SAH. Samples were obtained at baseline following surgical repair of SAH, and again at DCI onset. CSF was sampled at the same time points from in situ external ventricular drains. Results: DCI was associated with significant elevations of soluble markers of endotheliopathy, including vascular adhesion protein-1, soluble fractions of endothelial cell adhesion molecules (CAMs), procoagulant tissue factor, and specific markers of glycocalyx injury, including syndecan- 1, and CD44. These phenomena were also associated with an elevation of both circulating and CSF matrix metalloproteinases, which are known to cleave components of the glycocalyx. Elevation of vascular CAM-1 in the CSF with DCI indicated these events were possibly associated with the breakdown of br
traumatic brain injury;subarachnoid hemorrhage;endothelial cell;glycocalyx;cerebral ischemia
Report Number
DRDC-RDDC-2017-P056 — External Literature
Date of publication
01 Sep 2017
Number of Pages
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