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Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage
1Department of Neurosurgery, Helsinki University Central Hospital, Finland. seppo.juvela@helsinki.fi
Journal of Neurosurgery
|March 4, 2000
Summary
Elevated endothelin (ET) levels correlate with delayed cerebral ischemia and vasospasm after subarachnoid hemorrhage (SAH). Higher ET concentrations predict ischemic symptoms and vasospasm, potentially worsening outcomes in hypertensive patients.
Area of Science:
- Neuroscience
- Cardiovascular Research
- Endocrinology
Background:
- Cerebral vasospasm and delayed ischemia are complex complications following subarachnoid hemorrhage (SAH).
- Endothelin (ET), a potent vasoconstrictor, is implicated as a key mediator in chronic vasospasm.
Purpose of the Study:
- To investigate the correlation between serial plasma endothelin (ET) concentrations and the development of ischemic symptoms.
- To examine the relationship between ET levels, angiographically confirmed vasospasm, and computerized tomography (CT) findings post-aneurysmal SAH.
Main Methods:
- Plasma endothelin-1 (ET-1) immunoreactivity was measured in 70 aneurysmal SAH patients and 25 healthy volunteers using an immunometric assay.
- Serial ET concentrations were analyzed in relation to clinical outcomes, angiographic vasospasm severity, and CT-detected cerebral infarction.
Main Results:
- Mean plasma ET concentrations did not differ between SAH patients and healthy volunteers overall.
- Significantly higher ET levels were observed in patients experiencing delayed cerebral ischemia, severe vasospasm, or larger cerebral infarctions.
- Elevated ET was particularly noted in the early (Days 0-5) and later (Days 6-14) post-SAH periods for these patient groups.
Conclusions:
- Plasma endothelin (ET) concentrations correlate with delayed cerebral ischemia and vasospasm following subarachnoid hemorrhage (SAH).
- High ET levels are predictive of ischemic symptoms and vasospasm, and may exacerbate ischemia in hypertensive patients.
- ET is likely a significant factor in the pathogenesis of vasospasm after SAH, though its precise role requires further investigation.