Literature DB >> 9183335

Intra-arterial nitrovasodilators do not increase cerebral blood flow in angiographically normal territories of arteriovenous malformation patients.

S Joshi1, W L Young, J Pile-Spellman, P Fogarty-Mack, R R Sciacca, L Hacein-Bey, H Duong, Y Vulliemoz, N Ostapkovich, T Jackson.   

Abstract

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 micrograms.kg-1.min-1, n = 7), nitroprusside (0.5 microgram.kg-1.min-1, n = 16) or nitroglycerin (0.5 microgram.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.

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Year:  1997        PMID: 9183335     DOI: 10.1161/01.str.28.6.1115

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  5 in total

1.  Maintained cerebrovascular function during post-exercise hypotension.

Authors:  Christopher K Willie; Philip N Ainslie; Chloe E Taylor; Neil D Eves; Yu-Chieh Tzeng
Journal:  Eur J Appl Physiol       Date:  2013-01-12       Impact factor: 3.078

2.  Effect of hypoxia on vasodilator responses to S-nitroso-N-acetylpenicillamine and levcromakalim in guinea pig basilar artery.

Authors:  Pouya Movahed; Edward D Högestätt; Jesper Petersson
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2003-03-25       Impact factor: 3.000

3.  Cerebral autoregulation of blood velocity and volumetric flow during steady-state changes in arterial pressure.

Authors:  Jie Liu; Yong-Sheng Zhu; Candace Hill; Kyle Armstrong; Takashi Tarumi; Timea Hodics; Linda S Hynan; Rong Zhang
Journal:  Hypertension       Date:  2013-09-16       Impact factor: 10.190

4.  Intraarterially administered verapamil as adjunct therapy for cerebral vasospasm: safety and 2-year experience.

Authors:  Lei Feng; Brian-Fred Fitzsimmons; William L Young; Mitchell F Berman; Erwin Lin; Beverly D L Aagaard; Hoang Duong; John Pile-Spellman
Journal:  AJNR Am J Neuroradiol       Date:  2002-09       Impact factor: 3.825

Review 5.  Reassessing the Role of Intra-Arterial Drug Delivery for Glioblastoma Multiforme Treatment.

Authors:  Jason A Ellis; Matei Banu; Shaolie S Hossain; Rajinder Singh-Moon; Sean D Lavine; Jeffrey N Bruce; Shailendra Joshi
Journal:  J Drug Deliv       Date:  2015-12-30
  5 in total

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