Nitric oxide synthase inhibition attenuates vasoactive response to spinal cord stimulation in an experimental cerebral vasospasm model


Goksel H., Karadag O., Turaclar U., Tas F., Oztoprak I.

ACTA NEUROCHIRURGICA, vol.143, no.4, pp.383-391, 2001 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 143 Issue: 4
  • Publication Date: 2001
  • Doi Number: 10.1007/s007010170094
  • Title of Journal : ACTA NEUROCHIRURGICA
  • Page Numbers: pp.383-391

Abstract

Background. The basic mechanism of delayed cerebral vasospasm following subarachnoid haemorrhage (SAH) has been intensively investigated. II is thought that nitric oxide (NO) is a basic mediator of the cerebral vasodilator mechanism. Previous clinical and experimental studies have shown a cerebral vasodilator effect of high cervical spinal cord stimulation (SCS) however, the mechanism of this effect is still controversial. We investigated the contribution of the vasodilator effect of NO to this mechanism in an experimental SAH model using rabbits.