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

Background. The basic mechanism of delayed cerebral vasospasm following sub arachnoid haemorrhage (SAH) has been intensively investigated. II is though t that nitric oxide (NO) is a basic mediator of the cerebral vasodilator me chanism. Previous clinical and experimental studies have shown a cerebral v asodilator effect of high cervical spinal cord stimulation (SCS) however, t he mechanism of this effect is still controversial. We investigated the con tribution of the vasodilator effect of NO to this mechanism in an experimen tal SAH model using rabbits. Method. 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 cervic al epidural electrode placement without SCS were performed before TDU. Grou p 3. TDU was performed before and after SCS on the fourth day of SAH in 8 r abbits. Group 4. In 8 animals, N-Nitro-L-Arginine Methyl Esther (L-NAME) wa s 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. Findings. The occurrence of vasospasm after SAH was demonstrated with signi ficant changes in TDU parameters (high peak systolic velocity and positive values of the degree of stenosis). In all SAH animals, SCS resulted in sign ificant vasodilation. Even after the injection of L-NAME, SCS still had a s ignificant vasodilatory effect in SAH animals, but there was also a signifi cant difference in CBF parameters in the SCS-only group when compared with the L-NAME treatment before SCS group. Interpretation. The mechanism of the cerebral vasodilatory effect of SCS re mains controversial. Our results revealed the contribution of a neurohumora l effect which can be partially prevented by use of an NO synthase inhibito r.