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(Stroke. 1975;6:172.)
© 1975 American Heart Association, Inc.

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Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction

ERWIN O. OTT M.D.¹; JACOB ABRAHAM M.D.²; JOHN STIRLING MEYER M.D.³; AMRIT N. ACHARI M.D., M.R.C.P.³; ANTHONY N. C. CHEE M.A.³; NINAN T. MATHEW M.D., F.R.C.P.(C)³

¹ Baylor College of Medicine and is presently in the Department of Neurology, University Clinic of Neurology and Psychiatry, Graz, Austria
² Baylor College of Medicine and the Department of Neurological Sciences, Christian Medical College Hospital Vellore, India
³ Department of Neurology, Baylor College of Medicine, Houston, Texas 77025

John Stirling Meyer, M.D., Professor and Chairman, Department of Neurology, Baylor College of Medicine, Houston, Texas 77025.

The possible role of displaced neurotransmitter acetylcholine (ACh) in dysautoregulation was examined after experimental regional cerebral infarction was produced by occluding the middle cerebral artery (MCA) in baboons. Regional cerebral blood flow (rCBF) was measured after intracarotid injection of ¹³³Xenon using the gamma camera. Autoregulation was tested with metaraminol or angiotensin infusion and the autoregulation index (A.I.) was calculated. Acetylcholinesterase (AChE) was measured in brain tissue of noninfarcted and infarcted hemispheres. Cerebral arteriovenous (A-V) differences for cholinesterase (ChE) were also measured. Regional dysautoregulation was found in infarcted gray matter and correlated with increased AChE levels in the same zones of cortex and basal ganglia. The time course of onset of dysautoregulation correlated with increased ChE uptake by the brain. Intravenous infusion of the cholinergic neurotransmitter blocker, scopolamine, restored autoregulation to the ischemic zones. Autoregulation appears to be a myogenic reflex, influenced by neurogenic and metabolic mechanisms.

Key Words: acetylcholine • autoregulation • cerebral infarction • cholinesterase • regional cerebral blood flow