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(Stroke. 1997;28:1115-1122.)
© 1997 American Heart Association, Inc.

Articles

Intra-arterial Nitrovasodilators Do Not Increase Cerebral Blood Flow in Angiographically Normal Territories of Arteriovenous Malformation Patients

Shailendra Joshi, MD; William L. Young, MD; John Pile-Spellman, MD; Patricia Fogarty-Mack, MD; Robert R. Sciacca, EngScD; Lotfi Hacein-Bey, MD; Hoang Duong, MD; Yvonne Vulliemoz, PhD; Noeleen Ostapkovich, REEG/EPT; Tara Jackson, BS

From the Departments of Anesthesiology (S.J., W.L.Y., P.F.-M., Y.V., N.O., T.J.), Neurological Surgery (W.L.Y., J.P.-S.), Radiology (W.L.Y., J.P.-S., L.H.-B., H.D.), Medicine (R.R.S.), and Pharmacology (Y.V.), College of Physicians and Surgeons, Columbia University, New York.

Correspondence to William L. Young, MD, P&S Box 46, Columbia University, College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032. E-mail WLY1{at}columbia.edu

Background and Purpose The mechanism of adaptation to chronic cerebral hypotension in normal brain adjacent to cerebral arteriovenous malformations (AVMs) is unknown. To clarify these mechanisms, we performed cerebral blood flow (CBF) studies in structurally and functionally normal vascular territories during 53 distal cerebral angiographic procedures in 37 patients with AVMs.

Methods CBF was measured using the superselective intra-arterial ¹³³Xe method before and after a 3-minute infusion of either verapamil (1 mg·min^-1, n=23), acetylcholine (1.33 µg·kg^-1·min^-1, n=7), nitroprusside (0.5 µg·kg^-1·min^-1, n=16) or nitroglycerin (0.5 µg·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 to 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 infused 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 absence of response to nitric oxide–mediated vasodilators. These data suggest that (1) the nitric oxide pathway probably is not involved in the adaptation to chronic cerebral hypotension in AVM patients and (2) if our findings in vessels remote from or contralateral to the AVM are applicable to vessels of patients with other forms of cerebrovascular disease, clinically relevant doses of intra-arterial nitrovasodilators may not be useful in the manipulation of cerebrovascular resistance.

Key Words: autoregulation • calcium channel blockers • cerebral blood flow • nitric oxide

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