title: Evidence for adaptive autoregulatory displacement in hypotensive cortical territories adjacent to arteriovenous malformations. Columbia University AVM Study Project.
abstract: We hypothesized that chronic hypotension in normal vascular territories fed by arteriovenous malformation pedicles may reset the lower limit of autoregulation and allow flow to remain constant over a lower pressure range. We studied the effect of increasing systemic mean arterial pressure (SMAP) with phenylephrine on cerebral blood flow using a novel technique. Fourteen patients undergoing 15 procedures were studied before endovascular embolization of arteriovenous malformations under neuroleptic conscious sedation. Mean pressures were transduced via a 1.5-F intracranial microcatheter, which was passed under fluoroscopic guidance into the target feeding artery. The microcatheter was positioned (unwedged) at a point that was relatively hypotensive to systemic pressure but that irrigated normal cortex on angiography; feeding mean arterial pressure (FMAP) and SMAP were recorded. A bolus of 133Xe in saline was injected into the microcatheter, and washout was recorded for 3 minutes by a scintillation detector placed over the vascular territory of the injected pedicle. SMAP was then increased approximately 25 mm Hg by phenylephrine infusion, a second bolus was given, and washout was recorded. After exclusion of the shunt spike, initial slope was calculated. The SMAP (mean +/- standard error) increased from 65 +/- 3 to 89 +/- 2 mm Hg (P < 0.0001), and FMAP increased from 46 +/- 3 to 63 +/- 3 mm Hg (P < 0.0001); cerebral blood flow did not change (40 +/- 2 to 40 +/- 2 ml/100 g per min, P = 0.9199). Dividing the cases on the basis of the baseline FMAP into a "severe" hypotensive group (FMAP = 38 +/- 2; n = 7) and a "moderate" hypotensive group (FMAP = 54 +/- 3; n = 8), cerebral blood flow did not change in either group during phenylephrine challenge. Chronic hypotension does not necessarily result in "vasomotor paralysis" with loss of the ability to vasoconstrict to acute increases in perfusion pressure. Instead, it appears to displace adaptively the lower limit of autoregulation in affected vascular territories by a shift of the autoregulatory curve to the left, conceptually analogous to the adaptive displacement seen with chronic hypertension and its treatment.
authors.affiliation: Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, New York.
authors.forename: W L
authors.initials: WL
authors.lastname: Young
authors.forename: J
authors.initials: J
authors.lastname: Pile-Spellman
authors.forename: I
authors.initials: I
authors.lastname: Prohovnik
authors.forename: A
authors.initials: A
authors.lastname: Kader
authors.forename: B M
authors.initials: BM
authors.lastname: Stein
mesh_terms: D000293:Adolescent; D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002533:Cerebral Angiography; D002540:Cerebral Cortex / Q000098:blood supply*; D004621:Embolization, Therapeutic; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007022:Hypotension / Q000503:physiopathology*; D002538:Intracranial Arteriovenous Malformations / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D014666:Vasomotor System / Q000503:physiopathology