Abstract
The glycocalyx is an important constituent of blood vessels located between the bloodstream and the endothelium. It plays a pivotal role in intercellular interactions in neuroinflammation, reduction of vascular oxidative stress, and provides a barrier regulating vascular permeability. In the brain, the glycocalyx is closely related to functions of the blood-brain barrier and neurovascular unit, both responsible for adequate neurovascular responses to potential threats to cerebral homeostasis. An aneurysmal subarachnoid hemorrhage (aSAH) occurs following rupture of an intracranial aneurysm and leads to immediate brain damage (early brain injury). In some cases, this can result in secondary brain damage, also known as delayed cerebral ischemia (DCI). DCI is a life-threatening condition that affects up to 30% of all aSAH patients. As such, it is associated with substantial societal and healthcare-related costs. Causes of DCI are multifactorial and thought to involve neuroinflammation, oxidative stress, neuroinflammation, thrombosis, and neurovascular uncoupling. To date, prediction of DCI is limited, and preventive and effective treatment strategies of DCI are scarce. There is increasing evidence that the glycocalyx is disrupted following an aSAH, and that glycocalyx disruption could precipitate or aggravate DCI. This review explores the potential role of the glycocalyx in the pathophysiological mechanisms contributing to DCI following aSAH. Understanding the role of the glycocalyx in DCI could advance the development of improved methods to predict DCI or identify patients at risk for DCI. This knowledge may also alter the methods and timing of preventive and treatment strategies of DCI. To this end, we review the potential and limitations of methods currently used to evaluate the glycocalyx, and strategies to restore or prevent glycocalyx shedding.
Highlights
Intracranial aneurysms (IAs) are a common vascular pathology affecting around 2.8% of the population (Vlak et al, 2011)
To the best of our knowledge, there is currently only one clinical study that reported glycocalyx assessment in association with delayed cerebral ischemia (DCI) (Bell et al, 2017). In this small observational study, plasma markers of glycocalyx disruption such as Syndecan-1 and CD44, a glycoprotein receptor for hyaluronan, as well as the levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were assessed in three patients who developed DCI following their a subarachnoid hemorrhage (aSAH)
To the best of our knowledge, there is currently only one clinical study that reported glycocalyx assessment in association with DCI (Bell et al, 2017). When these were compared to a healthy population, it was found that the occurrence of aSAH was associated with increased plasma levels of Syndecan-1 and CD44, as well as ICAM-1 and VCAM-1 (Bell et al, 2017)
Summary
Intracranial aneurysms (IAs) are a common vascular pathology affecting around 2.8% of the population (Vlak et al, 2011). A delayed response to EBI commonly presents between 4 and 10 days following ictus, and occurs in around 30% of aSAH (Geraghty and Testai, 2017; Peeyush Kumar et al, 2019). This response is called delayed cerebral ischemia (DCI), defined as the development of a new neurological deficit, or a decrease in the Glasgow Coma Scale by two or more points lasting for at least 1 h after exclusion of other complications (Vergouwen et al, 2010). DCI strongly affects the outcome of aSAH, as it increases morbidity and mortality rates among aSAH patients, and prolongs hospital stays
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