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Endothelial cell activation after subarachnoid hemorrhage.
Catharina J M Frijns1, Gabriël J E Rinkel, Domenico Castigliego
1Department of Neurology, University Medical Center Utrecht, Utrecht, The Netherlands. C.J.M.Frijns@azu.nl
Neurosurgery
|May 23, 2002
Summary
Markers of endothelial cell activation, ED1-fibronectin (ED1-fn) and von Willebrand factor (vWf), are elevated after subarachnoid hemorrhage (SAH). These levels correlate with patient condition and increase after surgery or ischemic events, suggesting a role in SAH pathogenesis.
Area of Science:
- Neuroscience
- Vascular Biology
- Critical Care Medicine
Background:
- Animal studies suggest endothelial cell activation contributes to cerebral ischemia following subarachnoid hemorrhage (SAH).
- Endothelial cell activation markers, ED1-fibronectin (ED1-fn) and von Willebrand factor (vWf), are potential indicators of vascular injury.
- Assessing these markers in SAH patients can elucidate their role in disease progression.
Purpose of the Study:
- To measure plasma concentrations of ED1-fn and vWf in patients with aneurysmal SAH.
- To investigate the relationship between these markers and initial clinical status, treatment, and delayed cerebral ischemia.
- To explore the dynamic changes in endothelial activation markers post-SAH.
Main Methods:
- Blood samples were collected from 27 patients with aneurysmal SAH.
- ED1-fn and vWf plasma concentrations were measured.
- Patients underwent surgical (19), endovascular (7), or no (1) treatment for aneurysms.
- Delayed cerebral ischemia was monitored in 12 patients.
Main Results:
- Initial ED1-fn and vWf levels were significantly higher in SAH patients compared to reference values.
- Elevated marker concentrations were associated with poorer initial clinical condition.
- Marker levels increased significantly after surgical intervention and following ischemic episodes.
Conclusions:
- Plasma concentrations of ED1-fn and vWf are elevated early after SAH.
- These elevations are linked to the patient's clinical condition upon admission.
- Increased concentrations post-surgery and post-ischemia suggest a dynamic role for endothelial activation in SAH.
- The precise causal role of endothelial activation in delayed cerebral ischemia remains to be determined.