Effects of Beta-Adrenergic Blockade on Cerebral Autoregulation and Chemical Vasomotor Control in Patients With Stroke

Autoregulation and chemical vasomotor control of cerebral blood flow (CBF) were measured in 14 patients with cerebral ischemia and infarction classified according to severity and anatomical location before and after intracarotid injection of the beta-adrenergic blocking agent, propranolol hydrochloride (PPL). Intracarotid injection of 1.45 μg per kilogram body weight per minute of PPL (average total dose 2 mg) was followed by a reduction in CBF and oxygen consumption and an increase of cerebrovascular resistance. Mean arterial blood pressure, intracranial venous pressure, and cerebrospinal fluid pressure were unchanged. Cerebral autoregulation was tested by raising and lowering cerebral perfusion pressure (CPP) by the use of a tilt-table. Chemical vasomotor control of CBF was tested by inhalation of 7% CO2 + air and voluntary hyperventilation. Following the injection of PPL, cerebrovascular resistance was significantly increased when autoregulation was tested by raising CPP. The autoregulation index decreased significantly during the head-down position and tended to increase during the head-up position, but the latter trend did not reach the level of statistical significance. The chemical regulation index was not altered by propranolol during changes of Paco2. These results support the view that beta-adrenergic innervation influences cerebral metabolism as well as exerting a tonic cerebral vasodilator tonus. Hence, intracarotid injection of PPL blocks the beta-adrenergic dilator tonus and CBF and oxidative metabolism decrease. Likewise, the ability of cerebral vessels to constrict is improved when CPP is increased since cerebral vasoconstrictor tonus is enhanced. When CPP is lowered, cerebral autoregulation is unchanged or worsens. Chemical regulation of CBF to changes in Paco2, is unchanged by beta blockade.