INTRAARTERIAL NITROVASODILATORS DO NOT INCREASE CEREBRAL BLOOD-FLOW IN ANGIOGRAPHICALLY NORMAL TERRITORIES OF ARTERIOVENOUS MALFORMATION PATIENTS

Background and Purpose The mechanism of adaptation to chronic cerebral hypotension in normal brain adjacent to cerebral arteriovenous malfor mations (AVMs) is unknown. To clarify these mechanisms, we performed c erebral blood flow (CBF) studies in structurally and functionally norm al vascular territories during 53 distal cerebral angiographic procedu res in 37 patients with AVMs. Methods CBF was measured using the super selective intra-arterial Xe-133 method before and after a 3-minute inf usion of either verapamil (1 mg.min(-1), n=23), acetyl choline (1.33 m u g.kg(-1).min(-1), n=7), nitroprusside (0.5 mu g.kg(-1).min(-1), n=16 ) or nitroglycerin (0.5 mu g.kg(-1).min(-1), n=7). Results Mean +/- SD systemic (76 +/- 13 mm Hg) and distal cerebral arterial (55 +/- 16 mm Hg; range, 20 to 97 mm Hg) pressures were not different among groups. Verapamil increased CBF (45 +/- 12 to 65 +/- 21 mL.100 g(-1).min(-)1 P < .001). There was no effect of acetylcholine (no change [46 +/- 9 t o 46 +/- 9 mL.100 g(-1).min(-1)], NS) or nitroglycerin(36 +/- 14 to 36 +/- 13 mL.100 g(-1).min(-1), NS). Nitroprusside decreased CBF (40 +/- 12 to 31 +/- 11 mL.100 g(-1). min(-1), P < .001). The percent change in CBF after drug administration was proportional to cerebral arterial pressure for verapamil only (r=.57, P = .0051). Conclusions When infu sed intra-arterially in clinically relevant doses in both hypotensive and normotensive normal vascular territories remote from an AVM nidus, calcium channel blockade caused vasodilation, but there was an absenc e of response to nitric oxide-mediated vasodilators. These data sugges t that (1) the nitric oxide pathway probably is not involved in the ad aptation to chronic cerebral hypotension in AVM patients and (2) if ou r findings in vessels remote from or contralateral to the AVM are appl icable to vessels of patients with other forms of cerebrovascular dise ase, clinically relevant doses of intra-arterial nitrovasodilators may not be useful in the manipulation of cerebrovascular resistance.