Akademik Veri Yönetim Sistemi
Acta Neurochirurgica, cilt.143, sa.3, ss.277-285, 2001 (SCI-Expanded)
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.