Mays B W, Freischlag J A, Eginton M T, Cambria R A, Seabrook G R, Towne J B
Division of Vascular Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
J Surg Res. 1999 Jun 1;84(1):35-9. doi: 10.1006/jsre.1999.5601.
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.
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.
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.
Ascorbic acid protected the artery from cigarette smoke-induced endothelial injury.
吸烟会损害动脉内皮依赖性乙酰胆碱舒张功能,这种损伤可能由氧自由基介导。本研究旨在探讨抗坏血酸(AA)治疗对这种损伤的影响。
将新西兰白兔(每组n = 6只)置于一个240立方英尺的气流室中,每天3小时,每周5天,持续8周。动物分为四组,分别喂食兔饲料和水或兔饲料以及添加了AA(250毫升/千克)的水。对照 - 吸烟兔组和抗坏血酸 - 吸烟兔组在3小时内暴露于机器人烟雾发生器产生的主流香烟烟雾中,而对照 - 不吸烟兔组和抗坏血酸 - 不吸烟兔组同样置于无烟雾的室内。8周结束时,处死兔子,取出其股浅动脉段,悬挂于张力换能器上,测定最大收缩力。其余血管环收缩至最大收缩力的50%,然后通过添加乙酰胆碱测定舒张功能。采用单因素方差分析对各组进行比较。
与对照 - 不吸烟兔(3.86±0.40克)相比,对照 - 吸烟兔(5.13±0.21克)和抗坏血酸 - 吸烟兔(6.24±0.46克)的血管环对氯化钾的平均收缩力增加(P < 0.05)。与对照 - 不吸烟兔相比,对照 - 吸烟兔血管环中乙酰胆碱依赖性舒张功能显著降低(乙酰胆碱,5×10⁻⁷摩尔/升:24.7±2.7%对55.3±8.0%;乙酰胆碱,7×10⁻⁷摩尔/升:27.5±2.3%对56.3±9.2%)。抗坏血酸 - 吸烟组(乙酰胆碱,5×10⁻⁷摩尔/升:61.8±12.4%;7×10⁻⁷摩尔/升:67.9±11.4%)与对照 - 吸烟组相比,舒张功能显著增加(P < 0.05)。对照 - 不吸烟组、抗坏血酸 - 不吸烟组和抗坏血酸 - 吸烟组之间血管环舒张的平均百分比无统计学差异。
抗坏血酸可保护动脉免受香烟烟雾诱导的内皮损伤。