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Cited by 871

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Vitamin C improves endothelium-dependent vasodilation in patients with non-insulin-dependent diabetes mellitus.

Open access
Ting, H H, Timimi, F K, Boles, K S, Creager, S J, Ganz, P, Creager, M A·1996·Journal of Clinical Investigation
DOI 10.1172/jci118394
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Abstract

Endothelium-dependent vasodilation is impaired in humans with diabetes mellitus. Inactivation of endothelium-derived nitric oxide by oxygen-derived free radicals contributes to abnormal vascular reactivity in experimental models of diabetes. To determine whether this observation is relevant to humans, we tested the hypothesis that the antioxidant, vitamin C, could improve endothelium-dependent vasodilation in forearm resistance vessels of patients with non-insulin-dependent diabetes mellitus. We studied 10 diabetic subjects and 10 age-matched, nondiabetic control subjects. Forearm blood flow was determined by venous occlusion plethysmography. Endothelium-dependent vasodilation was assessed by intraarterial infusion of methacholine (0.3-10 micrograms/min). Endothelium-independent vasodilation was measured by intraarterial infusion of nitroprusside (0.3-10 micrograms/min) and verapamil (10-300 micrograms/min). Forearm blood flow dose-response curves were determined for each drug before and during concomitant intraarterial administration of vitamin C (24 mg/min). In diabetic subjects, endothelium-dependent vasodilation to methacholine was augmented by simultaneous infusion of vitamin C (P = 0.002); in contrast, endothelium-independent vasodilation to nitroprusside and to verapamil were not affected by concomitant infusion of vitamin C (P = 0.9 and P = 0.4, respectively). In nondiabetic subjects, vitamin C administration did not alter endothelium-dependent vasodilation (P = 0.8). We conclude that endothelial dysfunction in forearm resistance vessels of patients with non-insulin-dependent diabetes mellitus can be improved by administration of the antioxidant, vitamin C. These findings support the hypothesis that nitric oxide inactivation by oxygen-derived free radicals contributes to abnormal vascular reactivity in diabetes.

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Metadata

Authors
Ting, H. H., Timimi, F. K., Boles, K. S., Creager, S. J., Ganz, P., & Creager, M. A.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1996-01-01
Volume
97
Issue
1
Pages
22-28
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci118394
OpenAlex
W1975974235
Cited by
871
References
4
FWCI
27.41
Type
journal article
Language
en
Open access
bronze

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