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.