THE IMPACT OF SYSTEMIC VASOCONSTRICTORS ON THE CEREBRAL-CIRCULATION OF ANESTHETIZED PATIENTS

Background: The effect of vasoconstrictors on intracerebral hemodynami cs in anesthetized patients is controversial. The influence of phenyle phrine and norepinephrine on the cerebral circulation was investigated in isoflurane- or propofol-anesthetized patients using transcranial D oppler ultrasonography. Methods: Forty patients were randomly assigned to have vasoconstrictor tests with norepinephrine or phenylephrine du ring either Isoflurane or propofol anesthesia. Blood flow velocities w ere simultaneously measured in the middle cerebral artery and ipsilate ral extracranial internal carotid artery. Baseline recordings were don e during stable anesthesia in a supine position (test 0). A second ser ies of measurements were performed after norepinephrine or phenylephri ne had increased mean arterial blood pressure by about 20% (test 1). W ith maintained norepinephrine or phenylephrine infusion, a final serie s of results were obtained after the increased mean arterial blood pre ssure was counteracted by a slightly head-up patient position (test 2) . Results: Both vasoconstrictors significantly increased mean flow vel ocities in the middle cerebral artery (norepinephrine: 43 +/- 11 cm/s to 49 +/- 11 cm/s; phenylephrine: 43 +/- 8 cm/s to 48 +/- 9 cm/s; +/- SD) and internal carotid artery (norepinephrine: 27 +/- 7 cm/s to 31 /- 8 cm/s; phenylephrine: 27 +/- 9 cm/s to 31 +/- 10 cm/s) in the isof lurane-but not in the propofol-anesthetized patients. In the head-up p osition, only small and insignificant flow velocity changes were obser ved in both cerebral arteries independent of the vasoconstrictor or ba ckground anesthetic. Conclusions: The results of the present study ind icate that norepinephrine and phenylephrine do not directly affect int racranial hemodynamics in anesthetized patients, but rather that hemod ynamic changes observed with vasoconstrictors reflect the effect of th e background anesthetic agents on cerebral pressure autoregulation.