Summary
Background: Arterial endothelium-dependent acetylcholine relaxation is impaired by smoking, and this injury may be mediated by oxygen free radicals. The purpose of this study was to examine the effect of ascorbic acid (AA) treatment on this injury. Materials and methods: New Zealand White rabbits (n = 6, each group) were placed in a 240-ft3 airflow chamber for 3 h per day, 5 days per week over an 8-week period. Animals were divided into four groups and fed rabbit chow and water or rabbit chow and AA (250 ml/kg)-supplemented water. The control-smoke rabbit group and the ascorbic acid-smoke rabbit group were exposed to mainstream cigarette smoke from a robotic smoke generator for the 3-h period, while the control-no smoke rabbit group and ascorbic acid-no smoke rabbit group were similarly placed in the chamber without smoke. At the end of 8 weeks, rabbits were sacrificed and segments of their superficial femoral arteries were suspended from tension transducers and the maximal contraction was determined. The remaining rings were contracted to 50% of the maximum and relaxation was determined by adding acetylcholine. Groups were compared using one-way ANOVA. Results: Rings from control-smoke (5.13 +/- 0.21 g) and AA-smoke rabbits (6. 24 +/- 0.46 g) exhibited increased mean contraction to KCl (P < 0. 05) compared to control-no smoke rabbits (3.86 +/- 0.40 g). Acetylcholine-dependent relaxation was significantly reduced in the rings from the control-smoke rabbits compared to control-no smoke rabbits (acetylcholine, 5 x 10(-7) M: 24.7 +/- 2.7% versus 55.3 +/- 8.0%; acetylcholine, 7 x 10(-7) M: 27.5 +/- 2.3% versus 56.3 +/- 9. 2%). The AA-smoke group (acetylcholine, 5 x 10(-7) M: 61.8 +/- 12. 4%; 7 x 10(-7) M: 67.9 +/- 11.4%) had significantly increased relaxation compared to the control-smoke group (P < 0.05). There was no statistical difference in the mean percentage ring relaxation between the control-no smoke, AA-no smoke, and AA-smoke groups. Conclusions: Ascorbic acid protected the artery from cigarette smoke-induced endothelial injury.
References
B W Mays, J A Freischlag, M T Eginton, R A Cambria, G R Seabrook, J B Towne