Background. Recent studies on the pathogenesis of cerebral vasospasm follow
ing subarachnoid haemorrhage (SAH) suggest a breakdown of the balance betwe
en the vasoconstrictor and vasodilator systems. A shortage of a major cereb
ral vasodilator, nitric oxide (NO), has been accused of causing this breakd
own. We investigated the effect of continuous intracisternal infusion of a
NO precursor, L-Arginine, in a rabbit SAH model.
Method. Three experimental groups were designated: Group 1 - Cerebral blood
flow (CBF) data was obtained via transorbital Doppler ultrasonography (TDU
) in 8 normal rabbits. Group 2 - Intracisternal catheter placement and TDU
study during saline infusion were performed in 8 animals at the 4(th) day o
f SAH, Group 3 - SAH occurred in 8 animals. 4 days later, L-Arginine was in
fused intracisternally for 1 hour, while TDU was performed before and durin
g infusion. CBF parameters which were obtained via TDU measurement or calcu
lations, were compared.
Findings. The results of TDU revealed significant vasospasm in all SAH anim
als, as well as resolution of vasospasm with L-Arginine infusion. After 20
minutes of infusion, a steady and sustained vasodilation was obtained in th
e third group. The analysis of CBF data revealed a significant difference i
n SAH values, and no difference in control animals.
Interpretation. Our results support the contribution of the "NO shortage" c
oncept in the pathogenesis of cerebral vasospasm and overconsumption of L-A
rginine during the post-SAH period may cause this shortage. L-Arginine trea
tment may be useful for the prophylaxis and treatment of cerebral vasospasm
. The intracisternal infusion method can eliminate the short action time di
sadvantage of L-Arginine.