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Cerebral autoregulation and vasomotor responsiveness to carbon dioxide were measured quantitatively in normal baboons and after intravertebral or intravenous of the beta-adrenergic blocking agent, propranolol hydrochloride (Inderal). Continuous measurements were made of cerebral blood flow (CBF: measured as bilateral internal jugular venous outflow using an electromagnetic flowmeter), cerebral perfusion pressure (CPP), arterial Po2 and Pco2 and venous Po2, cerebral arteriovenous oxygen difference and endotracheal Pco2. The autoregulation index (A.I. = deltaCBF/deltaCPP) and the chemical index (C.I.= deltaCBF/deltaPaco2), were used as quantitative measures.

Baboons anesthetized with halothane and N2O/O2 were given an intravenous steroid anesthetic (Althesin; Glaxo Laboratories Ltd., U.K.). The drug bolus was labeled with 99mTc, and the time from central venous injection to peak radioactivity in the brain was designated drug brain arrival (DBA-peak). The electroencephalogram slowed 1.2 +/- 0.9 s after DBA-peak (P greater than 0.2), and approximately 2 s after DBA-peak, internal carotid blood flow (ICarBF) decreased and calculated internal carotid vascular resistance (ICarVR) rose. During this 2-s delay in the cerebrovascular response to the arrival of a cerebral metabolic depressant in the brain, the decrease in mean cortical Pco2 was calculated to be less than 0.26 mmHg from cortical CO2 solubility, and less than 0.32 mmHg from cortical CO2 diffusivity, which indicated that mean cortical Pco2 changes do not control cerebral blood flow (CBF). The unaltered time course of the changes in EEG, ICarBF, and ICarVR after acute cervical sympathectomy and alpha-adrenergic receptor blockade excluded the involvement of the sympathetic nervous system in the vasoconstrictor response. Intracarotid Althesin showed that the cerebral vasoconstriction was not a direct effect of the drug. The postulated link between the effects of Althesin on CBF and cerebral metabolism remains to be elucidated but is probably indirect, involving the brainstem.

This study presents ultrastructural confirmation of the embolic method of producing an ischemic lesion. The embolic method was shown to produce more advanced parenchymal changes than those reported for the same postocclusion period following vascular clipping. With this method there was less alteration in the morphological intergrity of occluded extraparenchymatous areas of the arterial bed, especially in the associated nerve bundles.

Cerebral blood flow (CBF) and metabolism were measured before and after withdrawal of 5 to 6 ml of cerebrospinal fluid (CSF) in 17 baboons. The measurements were made before and after infusion of tyrosine, the precursor amino acid of the putative neurotransmitters, dopamine and norepinephrine, in the brain. The same observations were made in another experimental group, i.e., before and after acute cerebral multiembolization induced by microfil emboli. In the steady state CBF was unaltered following reduction of intracranial pressure by removal of CSF. After infusion of tyrosine, CBF was decreased, and cerebrovascular resistance increased significantly on removal of CSF. Cerebral embolization did not influence changes in CBF at reduced intracranial pressure. It appears that the cerebral resistance vessels constrict following reduction of intracranial pressure by removal of CSF and that cerebrospinal fluid pressure-CBF autoregulatory mechanisms are resistant to cerebral ischemia induced by middle cerebral artery embolization.

Investigations concerned with the pathogenesis of hypertensive encephalopathy have reported two opposing changes in cerebral hemodynamics during induced hypertension: (1) vasospasm or vasoconstriction of the leptomeningeal arteries and (2) increase of cerebral blood flow which has been termed "breakthrough" of the cerebral autoregulation. To resolve this apparent conflict, continuous measurements of focal cerebral flow and oxygen availability were made in 17 baboons by the use of implanted platinum electrodes placed in both gray and white matter during induced hypertension. Autoregulation was initially well maintained in gray matter followed by "breakthrough" but the autoregulatory response was poorly maintained in the cerebral white matter. The vasoconstriction of the leptomeningeal arteries reported in earlier investigations from observations made through a skull window appears to be due to a marked autoregulatory response to hypertension rather than vasospasm. The autoregulatory response appears to be efficient in gray matter but relatively deficient in white matter.