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Journal article

Sodium Nitroglycerin Induces Cerebrovascular Vasodilation in Patients with Ischemic Heart Disease

Abstract

Aging patients with ischemic heart disease (IHD) have impaired cerebrovascular vasodilation in response to hypercapnia, but whether this is due to endothelial dysfunction or impairment in the vascular smooth muscle remains unknown. Further, despite being a standard drug given to patients with cardiovascular disease, the role of an exogenous nitric oxide donor (sodium nitroglycerin – NTG, which acts independently of the endothelium) in the cerebrovasculature in these patients is not known. This study tested the hypothesis that age and IHD impair nitric oxide‐mediated dilation (sodium nitric oxide, 0.4 mg spray) of the nine larger cerebral arteries in the Circle of Willis (3 Tesla MRI), as well as mean flow velocity [transcranial Doppler ultrasound; right middle cerebral artery (MCA)] and calculated MCA cerebral blood flow. These measures were made in groups of IHD (n=10, 49–77 years), older controls (CTL; n=5, 51–78 years) and young healthy (YH; n=10, 20–26 years) individuals. Compared to baseline, right MCA velocity [V (cm/s)] decreased similarly in all three groups [ΔIHD: −5.8 ± 5.0 cm/s; ΔCTL: −5.8 ± 3.2 cm/s; ΔYH: −6.3 ± 4.4: all p<0.05 versus baseline; mean ± S.D.]. However, a main effect of drug indicated that NTG induced artery dilation in all six basal and the three extracranial arteries [average range of cross sectional area values for all vessels provided here: BL: 3.3 – 16.5 mm 2 ; NTG: 3.9 – 17.9 mm 2 , p<0.05, mean], and this dilation was similar across all 3 groups [e.g. right MCA CSA – ΔIHD: 1.3 ± 1.4 mm 2 ; ΔCTL: 0.7 ± 1.2 mm 2 ; ΔYH: 1.3 ± 0.9 mm 2 , p>0.05 versus baseline; mean ± S.D.]. As a result, NTG exerted no change in MCA blood flow versus baseline. These results demonstrate that age and IHD have little impact on vascular smooth muscle responses to exogenous nitric oxide. Support or Funding Information Supported by Canadian Institute for Health Research (201503MOP‐342412‐MOV‐CEEA) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Authors

Schulz JM; Al‐Khazraji BK; Vording JL; Shoemaker JK

Journal

The FASEB Journal, Vol. 32, No. S1, pp. 712.8–712.8

Publisher

Wiley

Publication Date

April 1, 2018

DOI

10.1096/fasebj.2018.32.1_supplement.712.8

ISSN

0892-6638
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