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Related Experiment Videos

Endothelial dysfunction in a primate model of cerebral vasospasm.

Brian A Iuliano1, Ryszard M Pluta, Carla Jung

  • 1Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.

Journal of Neurosurgery
|April 17, 2004
PubMed
Summary

Subarachnoid hemorrhage (SAH) causes endothelial dysfunction, impairing cerebral vasomotility. This study in primates shows SAH-induced vasospasm disrupts normal endothelial responses, highlighting its role in the condition.

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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Pharmacology

Background:

  • Endothelial vasomotility abnormalities are implicated in various conditions.
  • The precise mechanism of endothelial dysfunction post-subarachnoid hemorrhage (SAH) remains incompletely understood.
  • In vivo studies on cerebral endothelial function following SAH and vasospasm are scarce.

Purpose of the Study:

  • To investigate endothelium-dependent responses in a primate model of cerebral vasospasm after SAH.
  • To assess the role of endothelial dysfunction in the development and maintenance of vasospasm.
  • To evaluate cerebrovascular responses to specific endothelium-acting agents.

Main Methods:

  • Seventeen adult male cynomolgus monkeys were utilized.
  • Cerebrovascular endothelium-dependent responses were measured via intracarotid infusions of acetylcholine, histamine, bradykinin, and Calcimycin.

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  • Cortical cerebral blood flow (CBF) and cerebrovascular resistance (CVR) were monitored 7, 14, and 21 days post-SAH.

    • Main Results:

    • Acetylcholine induced significant increases in CBF and reductions in CVR in control animals.
    • These acetylcholine-induced responses were abolished in animals 7 days post-SAH with confirmed vasospasm.
    • Calcimycin showed altered effects in SAH animals, indicating endothelial dysfunction.

    Conclusions:

    • Endothelial dysfunction significantly contributes to vasospasm following SAH.
    • The observed changes in vascular responses suggest a critical role for endothelial cells in SAH-induced cerebral vasospasm.
    • Findings support in vitro observations of endothelial denudation effects in vivo.