1 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas; Department of Neurosurgery, University of Kyoto, Kyoto, Japan
Reprint requests to: John Stirling Meyer, M.D., Professor and Chairman, Department of Neurology, Baylor College of Medicine, 1200 Moursund Avenue, Houston, Texas 77025
Cerebral autoregulation was studied in the baboon by increasing and decreasing cerebral perfusion pressure (CPP) before and after intravenous administration (1.5 mg per kilogram) of a long-acting alpha adrenergic blocker, phenoxybenzamine (PBZ). Likewise, cerebral vasomotor reactivity to changes of arterial carbon dioxide tension (PaCO2) was examined before and after PBZ. In order to permit quantitative analysis, cerebral autoregulation (A.I.) and chemical vasomotor reactivity (C.I.) were expressed as indices where A.I.= Following the intravenous injection of PBZ, cerebral autoregulatory vasoconstriction was impaired as CPP was increased. Cerebral vasomotor reactivity to changes in PaCO2 was altered both during hyperventilation hypocapnia (HV) and hypercarbia induced by inhalation of 5% carbon dioxide if alterations of CPP brought about by these procedures were taken into consideration. During hypocapnia C.I. was reduced 30% and during hypercarbia C.I. was increased 10%. It is concluded that PBZ reduces the vasoconstrictor tonus of cerebral vessels during hypocapnia and raised CPP. It also enhances the vasodilator response to CO2 inhalation.
© 1974 American Heart Association, Inc.
Neurogenic Control of Cerebral Blood Flow in the Baboon. Effects of Alpha Adrenergic Blockade With Phenoxybenzamine on Cerebral Autoregulation and Vasomotor Reactivity to Changes in PaCO2
2 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas
3 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas; Department of Surgery, Kobe University School of Medicine, Kobe, Japan
4 Department of Neurology, Baylor College of Medicine, and the Baylor-Methodist Center for Cerebrovascular Research, Houston, Texas; Department of Neurology, Osaka City University, Osaka, Japan
CBF/
CPP and C.I.=
CBF/
PaCO2.
Key Words: vasoconstriction vasodilatation hypacapnia hypercapnia adrenergic CBF control
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