Endothelin-1 may act as a trigger in the early stages of cerebral vasospasm, but its maintenance at later stages appears independent of endothelin-1.
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Endothelin-1 may trigger early vasospasm in this model; leaves open later mechanisms and any clinical translation.
Cerebral vasospasm was induced in adult mongrel dogs by a two-hemorrhage method. The basilar arteries were quickly frozen after careful removal of surrounding blood clot and their level of immunoreactive endothelin-1, a strong vasoconstrictor produced by the endothelial and vascular smooth-muscle cells, was measured by sandwich-enzyme immunoassay. The levels of immunoreactive endothelin-1 (mean +/- standard deviation) were 112.9 +/- 7.0 pg/mg protein prior to vasospasm, 180.4 +/- 24.7 pg/mg protein on Day 2 after vasospasm, and 115.0 +/- 24.0 pg/mg protein on Day 7, showing a significant increase (p less than 0.01) in immunoreactive endothelin-1 only on Day 2. In addition, vasospasm was moderately reversed by the topical application of monoclonal antibody against endothelin-1 on Day 2 but rather resistant to topical monoclonal antibody on Day 7. It is suggested that endothelin-1 could act as a trigger in the early stages of cerebral vasospasm, but that the maintenance of cerebral vasospasm at later stages might be independent of endothelin-1.
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Yamaura et al. (1992) studied this question.
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