Abstract
Endothelin-1 (ET-1) is known to be a vasocontractor peptide derived from the endothelium and to be involved in the pathogenesis of cerebrovascular disease (CVD). Plasma thrombomodulin (TM) is an endothelial cell marker which may reflect endothelial damage. In order to examine whether or not the antiplatelet agent, Cilostazol, could reduce the endothelial damage in CVD during the chronic stage, 25 patients with cerebral thrombosis at the chronic stage were given 400 mg of Ciloatazol every day for 2 weeks. We measured the levels of ET-1 and TM in the plasma before and after the administration. The plasma ET-1 level was significantly decreased from basal values of 2.16 ± 0.68 pg/ml to 1.75 ± 0.80 pg/ ml (p < 0.05). In addition, the reductions of the plasma levels of ET-1 following Cilostazol administration were significantly higher in CVD with diabetes mellitus (0.78 ± 0.51 pg/ml, p <0.05) than in CVD without diabetes mellitus (0.10 ± 0.28 pg/m1). On the other hand, no significant change in TM was noted between the values of 2.86 ± 0.72 FU/ml before and 2.85 ± 0.77 FU/ml after Cilostazol and administration. CVD with diabetes mellitus revealed significantly higher levels of TM (2.33 ± 0.75 FU/ml, P <0.05) than those without diabetes mellitus (1.91 ± 0.49 FU/ml). Cilostazol significantly reduced the plasma level of ET-1 in CVD. It is concluded therefore that Cilostazol did not exert a protective effect on thrombotic damage of the endothelium, but may reduce the induction of ET-1 from the endothelium through its inhibition of cyclic adenosine monophosphate hydrolysis.
