EVIDENCE FOR ADAPTIVE AUTOREGULATORY DISPLACEMENT IN HYPOTENSIVE CORTICAL TERRITORIES ADJACENT TO ARTERIOVENOUS-MALFORMATIONS

WE HYPOTHESIZED THAT chronic hypotension in normal vascular territorie s fed by arteriovenous malformation pedicles may reset the lower limit of autoregulation and allow flow to remain constant over a lower pres sure range. We studied the effect of increasing systemic mean arterial pressure (SMAP) with phenylephrine on cerebral blood flow using a nov el 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 g uidance into the target feeding artery. The microcatheter was position ed (unwedged) at a point that was relatively hypotensive to systemic p ressure but that irrigated normal cortex on angiography; feeding mean arterial pressure (FMAP) and SMAP were recorded. A bolus of Xe-133 in saline was injected into the microcatheter, and washout was recorded f or 3 minutes by a scintillation detector placed over the vascular terr itory of the injected pedicle. SMAP was then increased almost-equal-to 25 mm Hg by phenylephrine infusion, a second bolus was given, and was hout was recorded. After exclusion of the shunt spike, initial slope w as calculated. The SMAP (mean +/- standard error) increased from 65 +/ - 3 to 89 +/- 2 mm Hg (P < 0.0001), and FMAP increased from 46 +/- 3 t o 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 (F MAP = 38 +/- 2; n = 7) and a ''moderate'' hypotensive group (FMAP = 54 +/- 3; n = 8), cerebral blood flow did not change in either group dur ing phenylephrine challenge. Chronic hypotension does not necessarily result in ''vasomotor paralysis'' with loss of the ability to vasocons trict to acute increases in perfusion pressure. Instead, it appears to displace adaptively the lower limit of autoregulation in affected vas cular territories by a shift of the autoregulatory curve to the left, conceptually analogous to the adaptive displacement seen with chronic hypertension and its treatment.