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.