Effect of neonatal 6-hydroxydopamine treatment on experimental vasospasm following a subarachnoid hemorrhage in the rat.

Abstract

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic cerebral arterial vasospasm. Systemic 6-hydroxydopamine (6-OHDA) treatment in the neonatal stage, which causes a depletion of noradrenaline (NA) from both sympathetic and central NA-containing nerve fibers, prevents the development of the late spasm phase, while the acute spasm occurs to the same extent as in normal animals. The occurrence of acute spasm can be prevented by lesioning in the mesencephalon of the ascending catecholamine fibers originating in the lower brainstem and projecting to the hypothalamus. It is suggested that 6-OHDA treatment results in the altered spasm pattern via its effect on catecholamine fibers projecting between the medullary A1 and A2 nuclei and the hypothalamus. The occurrence of acute but not late spasm indicates that there is a different pathway underlying the two spasm phases.