title: Nitric oxide synthase inhibition attenuates vasoactive response to spinal cord stimulation in an experimental cerebral vasospasm model.
abstract: BACKGROUND
  The basic mechanism of delayed cerebral vasospasm following subarachnoid haemorrhage (SAH) has been intensively investigated. It 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.
  
  
  METHODS
  Four experimental groups, were designated: Group 1. Cerebral blood flow (CBF) was evaluated by transcranial Doppler ultrasonography (TDU) in 8 rabbits. Group 2. In 4 animals, intracisternal saline injection and cervical epidural electrode placement without SCS were performed before TDU. Group 3. TDU was performed before and after SCS on the fourth day of SAH in 8 rabbits. Group 4. In 8 animals, N-Nitro-L-Arginine Methyl Esther (L-NAME) was administered intracisternally on the fourth day of SAH, at a dose of 0.6 mg/kg, 45 minutes before SCS. CBF parameters, obtained via measurements or calculations from TDU data, were compared.
  
  
  RESULTS
  The occurrence of vasospasm after SAH was demonstrated with significant changes in TDU parameters (high peak systolic velocity and positive values of the degree of stenosis). In all SAH animals, SCS resulted in significant vasodilation. Even after the injection of L-NAME, SCS still had a significant vasodilatory effect in SAH animals, but there was also a significant difference in CBF parameters in the SCS-only group when compared with the L-NAME treatment before SCS group.
  
  
  CONCLUSIONS
  The mechanism of the cerebral vasodilatory effect of SCS remains controversial. Our results revealed the contribution of a neurohumoral effect which can be partially prevented by use of an NO synthase inhibitor.
authors: Department of Neurosurgery, Cumhuriyet University, School of Medicine, Sivas, Turkey.
authors: H M
authors: HM
authors: Göksel
authors: O
authors: O
authors: Karadag
authors: U
authors: U
authors: Turaçlar
authors: F
authors: F
authors: Taş
authors: I
authors: I
authors: Oztoprak
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging / Q000187:drug effects; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy; D005260:Female; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D010092:Oximetry; D011817:Rabbits; D013116:Spinal Cord / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology*; D013345:Subarachnoid Hemorrhage / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D017585:Ultrasonography, Doppler, Transcranial; D014664:Vasodilation / Q000187:drug effects*; D020301:Vasospasm, Intracranial / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D019331:NG-Nitroarginine Methyl Ester