Effect of selective lesions of medullary catecholamine nuclei on experimental cerebral vasospasm in the rat.
Intracisternal injection of blood in the rat induces an angiographically demonstrable, biphasic cerebral vasospasm of the vertebrobasilar system, with a maximal acute spasm at 10 min and a maximal late spasm at 2 days after the subarachnoid hemorrhage (SAH). Selective lesioning of the A1 nuclei in the medulla oblongata prior to the SAH prevents the development of the late spasm, but the acute spasm develops to the same extent as in sham-lesioned animals. Lesions of the medullary A2 nuclei not only prevent the development of both acute and late spasm, but give rise to a dilatation of the vertebrobasilar arteries at day 2 post-SAH. The study indicates that both the A1 and A2 nuclei participate in the development of vasospasm post-SAH. The contrasting patterns of spasm after A1 and A2 lesions suggest a different mechanism for acute and late spasm.
D000320:Adrenergic Fibers / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D006892:Hydroxydopamines; D007031:Hypothalamus / Q000032:analysis; D002546:Ischemic Attack, Transient / Q000209:etiology*; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D009638:Norepinephrine / Q000032:analysis; D016627:Oxidopamine; D011674:Pulse; D051381:Rats; D011919:Rats, Inbred Strains; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology
D006892:Hydroxydopamines; D016627:Oxidopamine; D009638:Norepinephrine