Endothelin in cerebrospinal fluid and plasma of patients in the early stage of ischemic stroke.

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Abstract
Background and Purpose Endothelin 1 (ET-1), a highly potent endogenous vasoactive peptide, exerts a sustained vasoconstrictive effect on cerebral vessels. Elevation of ET-1 in plasma has been reported 1 to 3 days 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 constriction 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 scans. Within 5 to 18 hours of stroke onset, lumbar puncture and blood samples were concomitantly obtained and tested; ET-1 levels in CSF and plasma of these patients were analyzed by radioimmunoassay and compared 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 stroke 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 infarcts (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 hours after stroke. No elevation was demonstrated in plasma at this time period. ET-1 may be used as an additional indicator of ischemic vascular 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 neuronal effect caused by ET-1 in the mechanism of the progression of brain ischemia.