Sodium nitroglycerin induces middle cerebral artery vasodilatation in young, healthy adults

Abstract

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. AbstractRecent 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.

Cerebral Vasodilator Property of Poly(ADP-Ribose) Polymerase Inhibitor (PJ34) in the Neonatal and Adult Mouse Is Mediated by the Nitric Oxide Pathway

“…NO-donors provoke a dilation of these arteries with a consecutive decrease in local mBFV because both CBF, and the downstream arteriolar resistance are maintained in absence of metabolic modification ( Figure 5 B). Previous studies showed the absence of metabolic stimulation illustrated by the absence of variation of the end-tidal partial pressure of CO 2 and thus of the arterial blood gases before and during exogenous NO-donor, avoiding any confounding sources of dilation elicited by hypercapnia [ 22 ]. The putative mechanism for the maintenance of arteriolar resistance could be the opposite action of the sympathetic nervous system (SNS) with proportionately greater vasoconstrictor effects on the downstream arterioles than on the conduit arteries.…”

Regulation of regional cerebral blood flow during graded reflex-mediated sympathetic activation via lower body negative pressure

“…Another possible mechanism involved in CBF regulation is nitric-oxide (NO)-mediated vasodilation. However, there is controversial evidence, with some studies supporting the role of NO in CBF regulation (30,33) and others suggesting a negligible role of NO (1,37,41). In addition, the cerebral vasculature is also well innervated with cholinergic fibers (10), although the role of the cholinergic system in CBF regulation remains unclear.…”

Vasodilatation by carbon dioxide and sodium nitroglycerin reduces compliance of the cerebral arteries in humans

“…The Coverdale et al, 2014Coverdale et al, , 2015Schulz et al, 2018;Verbree et al, 2014) and that hypercapnia also dilates the distal MCA vascular bed, these findings indicate that the reductions in Ci were largely accounted for by dilatation of the larger cerebral arteries. Further, these findings highlight differences in the effect of vasodilatation on vascular compliance in the peripheral and cerebral vascular beds.…”

“…We note that the change in Ci with hypercapnia cannot be accounted for by changes in BP. Further, with a single sublingual spray of SNG, Schulz et al (2018) observed an increase in MCA crosssectional area. Although the time course of MCA dilatation was not reported in the previous investigation, the current data are consistent with observations that internal carotid artery peak dilatation occurs approximately 7 min following sublingual nitroglycerin delivery and the dilatation persisted for 10 min (Carr et al, 2020).…”

“…In contrast, SNG appears to dilate the large cerebral conduit arteries (i.e., large cerebral arteries and pial arteries) but not the downstream cerebral vasculature (i.e., intra-parenchymal arterioles). This notion is based on previous reports of nitroglycerin-mediated pial artery dilatation in dogs (Ishiyama et al, 1994), basilar artery dilatation in dogs (Kistler et al, 1979), and MCA dilatation in humans (Hansen et al, 2007;Schulz et al, 2018). Despite large cerebral artery dilatation, observation of (i) reduced MCAv (Bednarczyk et al, 2002;Dahl et al, 1989;Schulz et al, 2018;White et al, 2000;Zuj et al, 2012), (ii) no change in CBF (Dahl et al, 1989;Schulz et al, 2018;von Essen et al, 1981;White et al, 2000) or regional changes in CBF (Bednarczyk et al, 2002), and…”