Vessel Wall Inflammation In The Pathogenesis Of Sah Vasospasm After The Role Of Clinical And Experimental Research

Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a complicated pathophysiological course caused by varied factors. The present study was undertaken to examine the changes of markers of endothelial dysfunction, coagulation factor, inflammatory mediators and vascular adhesion molecules in blood of the internal jugular vein in patients with SAH. The results showed that plasminogen activator inhibitor-I (PAL-i), interleukin-6(IL-6), thromb in- antithrombin III complex(TAT) and platelet activating factor(PAF) concentrations increased within first 3 days after SAH and remained elevated up to 14 days, P- selectin and intercellular adhesion molecule-1(ICAM-l) levels increased within 9 days after SAH. While it was showed a transient increase with soluble thrombomodullin(sTM), interleukin-l P (IL-i P ) and vascular cell adhesion molecuie-l(VCAM-1) between 4-9 days and E-selectin within first 3 days after SAH, tumor necrosis factor- a (TNF- a) remained unchanged. The patients with synptomatic vasospasrn displayed the higher levels of PAL-i, sTM, TAT, IL-I P, IL-6, PAF, ICAM-1 and VCAM-l than those without synptomatic vasospasm. Moreover, ICAM-1 levels have statistically significant correlation with PAl-i, TAT, IL-6 and PAF, the correlations were also observed between PAL-i and TAT, and between IL-6 and PAF. These results suggest that the cerebral vasospasm after SAH is the pathophysiological consequence initiated by the blood surround spasmodic artery and may be developed by varied interactive factors, including vascular endothelial dysfunction, releasing of inflammatory mediators, blood hypercoagulant state and upregulated expression of vascular adhsion molecule, in which the inflammatory reaction in artery wall may be an inevitable pathological course.