Vitamins C and E inhibit O2- production in the pig coronary artery

• Published in: Circulation (New York, N.Y.) Vol. 96; no. 10; pp. 3593 - 3601
• Main Authors: NUNES, G. L, ROBINSON, K, KALYNYCH, A, KING, S. B, SGOUTAS, D. S, BERK, B. C
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 18.11.1997; American Heart Association, Inc
• Subjects: Animals; Arteries - drug effects; Arteries - metabolism; Ascorbic Acid - blood; Ascorbic Acid - pharmacology; Biological and medical sciences; Cholesterol - blood; Coronary Vessels - drug effects; Coronary Vessels - metabolism; Female; General and cellular metabolism. Vitamins; Medical sciences; Pharmacology. Drug treatments; Superoxides - metabolism; Swine; Vitamin E - blood; Vitamin E - pharmacology; Oxygen; Vitamin; Coronary artery; Instrumentation therapy; Cardiovascular disease; Exploration; α-Tocopherol; Instrumental dilatation; Antioxidant; Coronary heart disease; Free radical; Pig; Retinol; Restenosis; Chemotherapy; Vertebrata; Mammalia; Treatment; Animal; Production; Complication; Artiodactyla; Ungulata
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.96.10.3593

We previously found in a pig coronary balloon injury model that vitamins C and E as well as probucol had beneficial effects on the vessel response to injury measured by morphometry These effects correlated with an inhibition in the ability to oxidize LDLs ex vivo, suggesting that the morphological response was due to the antioxidant effect of the treatments. In the present study, the production of O2- by vessels 14 days after balloon injury was determined and correlated with circulating and tissue levels of vitamins C and E. Twenty-five domestic pigs were divided into four groups: control (n=7), vitamin C (500 mg/d, group C, n=6), vitamin E (1000 IU/d, group E, n=6), and vitamins C and E (500 mg/d and 1000 IU/d, group C+E, n=6). Vitamins were administered 7 days before oversized balloon injury of the left anterior descending coronary artery (LAD) and continued for 14 days after injury. Vitamin C and E concentrations were determined in plasma and lymphocytes as an index for tissue levels. Vessels were harvested after animals were killed, and O2- production was measured by lucigenin chemiluminescence. O2- production by the injured LAD was 2.5-fold greater than O2- production by the uninjured LAD or right coronary artery (RCA). The increase in O2- was caused primarily by cells present in the media and neointima. All vitamin-treated groups showed significantly decreased O2- production in both the RCA and LAD (approximately 45% inhibition) relative to vessels in the control, untreated group. There was a significant correlation between LAD O2- production and lymphocyte vitamin E levels. The present study is the first to show increased O2- production in injured vessels and to demonstrate that antioxidant vitamins reduce O2- production. These results suggest that beneficial effects of antioxidant vitamins in coronary artery disease are related, in part, to alterations in vessel redox state.