Background:Endothelial cell activation may be connected with the pathogenesis of delayed cerebral ischaemia(DCI)after subarachnoid haemorrhage(SAH).Aim:To assess the relationship between serial concentrations of circulating markers of endothelial cell activation(soluble intercellular adhesion molecule-1,soluble platelet selectin(sP-selectin),soluble endothelial selectin,ED1-fibronectin,Von Willebrand Factor(VWF)and VWF propeptide)and development of DCI.Methods:687 blood samples were collected from 106 consecutive patients admitted within 72 h after onset of SAH.Changes in levels were analysed in the last sample before and in the first sample after the onset of DCI(n = 30),and in subgroups with DCI occurring within 24 h after treatment of the aneurysm(n = 12)or unrelated to treatment of the aneurysm(n = 18).Patients without DCI(n = 56)served as controls.Results:Concentrations of sP-selectin,but not of the other markers,were found to increase considerably after DCI unrelated to treatment of the aneurysm(increase 25 ng/ml,95%CI 8 to 43),whereas they tended to decrease in the control patients without DCI(decrease 13 ng/ml,95%CI-28 to 2.4).Surgery was found to profoundly influence the levels of the markers irrespective of the occurrence of DCI.Conclusion:The rise in sP-selectin level during DCI is suggested to be the result of platelet activation,as levels of the other markers of endothelial cell activation were not increased after DCI unrelated to treatment.Whether a causal role of platelet activation is implicated in the development of DCI should be determined in further studies in which the relationship between concentrations of markers and treatment is taken into account. Background: Endothelial cell activation may be connected with the pathogenesis of delayed cerebral ischaemia (DCI) after subarachnoid haemorrhage (SAH). Aim: To assess the relationship between serial concentrations of circulating markers of endothelial cell activation (soluble intercellular adhesion molecule-1, soluble Platelet selectin (sP-selectin), soluble endothelial selectin, ED1-fibronectin, Von Willebrand Factor (VWF) and VWF propeptide) and development of DCI. Methods: 687 blood samples were collected from 106 consecutive patients admitted within 72 h after onset of SAH .Changes in levels were analysed in the last sample before and in the first sample after the onset of DCI (n = 30), and in subgroups with DCI releases within 24 h after treatment of the aneurysm (n = 12) or unrelated to treatment of the aneurysm (n = 18). Pats without DCI (n = 56) served as controls. Results: Concentrations of sP-selectin, but not of the other markers, were found to increase inhibitor after DCI unrelated to treatment of the aneurysm (increase 25 ng / ml, 95% CI 8 to 43), when they tended to decrease in the control patients without DCI (decrease 13 ng / ml, 95% CI- 28 to 2.4) .Surgery was found to profoundly influence the levels of the markers irrespective of the occurrence of DCI. Confc: The rise in sP-selectin level during DCI is suggested to be the result of platelet activation, as levels of the other markers of endothelial cell activation were not increased after DCI unrelated to treatment. Whih a causal role of platelet activation is implicated in the development of DCI should be determined in further studies in which the relationship between concentrations of markers and treatment is taken into account.