Increased sensitivity of the basilar artery to norepinephrine and 5-hydroxytryptamine following experimental subarachnoid hemorrhage.

The reactivity of rabbit basilar artery to norepinephrine and 5-hydroxytryptamine was tested in vitro three days following cisternal injection of 1.0 ml autologous blood to simulate subarachnoid hemorrhage. Following this treatment the artery became three to five times more sensitive to norepinephrine compared with vessels from untreated animals. This was reflected in a parallel shift of the log dose-response curve towards lower concentrations of norepinephrine in a way resembling that seen after cocaine treatment of sympathectomy and interpreted as a prejunctional supersensitivity of the vascular alpha-receptors. The injection of blood also increased the amount of vasoconstriction with 5-hydroxytryptamine to a level which was three times higher than that obtained in untreated vessels. The results suggest one type of mechanism whereby monoamines might be involved in cerebral vasospasm following subarachnoid hemorrhage.