Bone and Joint Institute
Document Type
Article
Publication Date
8-1-2018
Journal
Experimental Physiology
Volume
103
Issue
8
First Page
1047
Last Page
1055
URL with Digital Object Identifier
10.1113/EP087022
Abstract
© 2018 The Authors Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society New Findings: What is the central question of this study? Nitric oxide causes dilatation in peripheral vessels; however, whether nitric oxide affects basal cerebral artery dilatation has not been explored. What is the main finding and its importance? This study demonstrated that vasodilatation occurs in the right middle cerebral artery in response to exogenous nitric oxide. However, blood velocity decreased and, therefore, overall cerebral blood flow remained unchanged. This study provides new insight into the role of nitric oxide in cerebral blood flow control. Abstract: Recent evidence indicates that basal cerebral conduit vessels dilate with hypercapnia, with a nitric oxide (NO) mechanism explaining one way in which parenchymal cerebral arterioles dilate. However, whether NO affects basal cerebral artery dilatation remains unknown. This study quantified the effect of an exogenous NO donor [sodium nitroglycerin (NTG); 0.4 mg sublingual spray] on the right middle cerebral artery (rMCA) cross-sectional area (CSA), blood velocity and overall blood flow. Measures of vessel CSA (7 T magnetic resonance imaging) and MCA blood velocity (transcranial Doppler ultrasound) were made at baseline (BL) and after exogenous NTG or placebo (PLO) administration in young, healthy individuals (n = 10, two males, age range 20–23 years). The CSA increased in the rMCA [BL, 5.2 ± 1.2 mm2; PLO, 5.4 ± 1.5 mm2; NTG, 6.6 ± 1.5 mm2, P < 0.05; mean ± SD]. Concurrently, rMCA blood velocity decreased from BL during NTG compared with PLO (BL, 67 ± 10 cm s−1; PLO, 62 ± 10 cm s−1; NTG, 59 ± 9.3 cm s−1, P < 0.05; mean ± SD]. However, total MCA blood flow did not change with NTG or PLO [BL, 221 ± 37.4 ml min−1; PLO, 218 ± 35.0 ml min−1; NTG, 213 ± 46.4 ml min−1). Therefore, exogenous NO mediates a dilatory response in the rMCA, but not in its downstream vascular bed.
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This work is licensed under a Creative Commons Attribution 4.0 License.
Notes
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Copyright 2018 The authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society
This article is originally available at:
Schulz, J. M, Al-Khazraji, B. K., & Shoemaker, J. K. (2018). Experimental Physiology. 2018;103:1047–105. DOI: https://doi.org/10.1113/EP087022