ENDOTHELIN IN CEREBROSPINAL-FLUID AND PLASMA OF PATIENTS IN THE EARLY-STAGE OF ISCHEMIC STROKE

Background and Purpose Endothelin 1 (ET-1), a highly potent endogenous vasoactive peptide, exerts a sustained vasoconstrictive effect on cer ebral vessels. Elevation of ET-1 in plasma has been reported 1 to 3 da ys after ischemic stroke. Since we assumed that a much faster and more intense response may be observed in the cerebrospinal fluid (CSF) and since an increase in concentration of ET-1 in the CSF may cause const riction of cerebral vessels and eventually influence the neurological outcome, we measured ET-1 values in the CSF within 18 hours of stroke onset and compared the values with those in the plasma. Methods Twenty -six consecutive patients with acute stroke were clinically evaluated according to the modified Matthew Scale and underwent two repeat CT sc ans. Within 5 to 18 hours of stroke onset, lumbar puncture and blood s amples were concomitantly obtained and tested; ET-1 levels in CSF and plasma of these patients were analyzed by radioimmunoassay and compare d with the levels of a control group of patients with no neurological disease. Results The mean CSF concentration of ET-1 in the CSF of stro ke patients was 16.06+/-4.9 pg/mL, compared with 5.51+/-1.47 pg/mL in the control group (P<.001). It was significantly higher in cortical in farcts (mean, 17.7+/-4.1 pg/mL) than in subcortical lesions (mean, 10. 77+/-4.1 pg/mL) (P<.001) and significantly correlated with the volume of the lesion (P=.003). The correlation between ET-1 levels in the CSF and the Matthew Scale score was less significant (P=.05). Plasma ET-1 level was not elevated in any group. Conclusions ET-1 is found to be significantly elevated in the CSF of stroke patients during the 18 hou rs after stroke. No elevation was demonstrated in plasma at this time period. ET-1 may be used as an additional indicator of ischemic vascul ar events in the early diagnosis of stroke. The dissimilarity between the CSF and plasma ET-1 concentrations may lead also to an hypothesis that there is a vasoconstrictive effect on the cerebral vessels or a n euronal effect caused by ET-1 in the mechanism of the progression of b rain ischemia.