The therapeutic effect of continuous intracisternal L-Arginine infusion on experimental cerebral vasospasm.

BACKGROUND: Recent studies on the pathogenesis of cerebral vasospasm following subarachnoid haemorrhage (SAH) suggest a breakdown of the balance between the vasoconstrictor and vasodilator systems. A shortage of a major cerebral vasodilator, nitric oxide (NO), has been accused of causing this breakdown. 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 4th day of SAH, Group 3--SAH occurred in 8 animals. 4 days later, L-Arginine was infused intracisternally for 1 hour, while TDU was performed before and during infusion. CBF parameters which were obtained via TDU measurement or calculations, were compared.
FINDINGS: The results of TDU revealed significant vasospasm in all SAH animals, as well as resolution of vasospasm with L-Arginine infusion. After 20 minutes of infusion, a steady and sustained vasodilation was obtained in the third group. The analysis of CBF data revealed a significant difference in SAH values, and no difference in control animals.
INTERPRETATION: Our results support the contribution of the "NO shortage" concept in the pathogenesis of cerebral vasospasm and overconsumption of L-Arginine during the post-SAH period may cause this shortage. L-Arginine treatment may be useful for the prophylaxis and treatment of cerebral vasospasm. The intracisternal infusion method can eliminate the short action time disadvantage of L-Arginine.