Effects of alpha adrenergic blockade on autoregulation and chemical vasomotor control of CBF in stroke.

Effects of Alpha Adrenergic Blockade on Autoregulation and Chemical Vasomotor Control of CBF in Stroke • Autoregulation and chemical vasomotor control of cerebral blood flow (CBF) were quantitatively tested in 19 patients with various types and sites of cerebral ischemia and infarction. The effect of alpha adrenergic blockade of cerebral vessels by phenoxybenzamine (PBZ) also was evaluated in more than half of the patients. No correlation was found between the degree of cerebral dysautoregulation and impairment of chemical vasomotor control of CBF. Patients with brainstem ischemia and infarction showed normal vasomotor reactivity of CBF to changes in Pa^,, despite the impairment of cerebral autoregulation during both induced hypotension and hyper ension. Following intracarotid injection of 10 mg PBZ, the degree of cerebral dysautoregulation lessened during induced hypotension but increased during induced hypertension. Chemical vasomotor control of CBF in response to changes in Pa^,, was not significantly altered by the PBZ injection. Changes in autoregulation index (a quantitative measure of cerebral autoregulation) after the infusion were compared with changes in chemical regulation index (a quantitative measure of cerebral vasomotor reactivity). Induced hypotension and hypercapnia yielded a proportional correlation between these two indexes, while induced hypotension and hypocapnia revealed a significant inverse correlation. This study demonstrates that cerebral autoregulation is influenced by the autonomic innervation of cerebral vessels. Alpha adrenergic blockade improves impaired autoregulation when cerebral perfusion pressure (CPP) is lowered but worsens it when CPP is raised, indicating that PBZ impairs the ability of cerebral vessels to constrict during induced hypertension and improves their ability to dilate during induced hypotension. This study also supports the view that chemical vasomotor control is regulated not directly by autonomic innervations of cerebral vessels but by a local controlling mechanism. Additional