Pharmacologic irreversible narrowing in chronic cerebrovasospasm in rabbits is associated with functional damage.
 We studied isolated basilar artery segments from a rabbit model of chronic cerebrovasospasm.
 Autologous blood placed around the basilar artery of rabbits killed 1, 2, 3, 4, 5, 6, 7, or 9 days later caused narrowing of the segments with a biphasic time course.
 The first (immediate) phase was reversed by intra-arterial papaverine; the second phase exhibited an increasing component of narrowing that was papaverine-insensitive.
 Based on the passive force/length curves, basilar artery segments became increasingly stiff over 9 days.
 By contrast, the segments' contractility decreased.
 Responses of the basilar artery segments were greater over the first few days, but then became less than that of saline-injected controls.
 Contractions in response to norepinephrine and potassium were reduced.
 Endothelium-based acetylcholine-induced vasodilation progressively diminished, as did the response to sympathetic nerve stimulation.
 There was a negative correlation between artery wall stiffness and contractility.
 The papaverine-insensitive component of angiographic narrowing correlated directly with loss of contractility and with artery wall stiffness.
 These results are consistent with the conclusion that increased artery wall stiffness is a primary determining factor in the arterial narrowing of chronic cerebrovasospasm.
