Walker H A, McGing E, Fisher I, Böger R H, Bode-Böger S M, Jackson G, Ritter J M, Chowienczyk P J
Cardiothoracic Centre, St. Thomas' Hospital, London, United Kingdom.
J Am Coll Cardiol. 2001 Aug;38(2):499-505. doi: 10.1016/s0735-1097(01)01380-8.
This study was designed to determine the effect of two weeks' treatment with L-arginine on the ratio of plasma L-arginine to asymmetric dimethylarginine (ADMA), oxidative stress, endothelium-dependent vasodilatation to acetylcholine, exercise performance and heart rate variability in men with stable angina.
The ratio of plasma L-arginine:ADMA has been proposed as a determinant of endothelium-dependent dilation; dietary supplementation with L-arginine has been shown to improve endothelium-dependent vasodilation and symptoms in some conditions.
Men (n = 40) with stable angina, at least one epicardial coronary artery with a stenosis >50% and a positive exercise test were randomized to receive L-arginine (15 g daily) or placebo for two weeks according to a double-blind parallel-group design. Plasma L-arginine, ADMA, 8-epi-prostaglandin F2alpha (a marker of oxidative stress) and forearm vasodilator responses to brachial artery infusion of nitroprusside and acetylcholine (+/-L-arginine) were measured. A standard Bruce protocol exercise test was performed before and at the end of the treatment period.
Plasma L-arginine increased after oral L-arginine, whereas ADMA remained unchanged, leading to an increase in the L-arginine/ADMA ratio of 62 +/- 11% (mean +/- SE, p < 0.01). Despite a significant enhancement in acetylcholine response by intra-arterial L-arginine at baseline, this response remained unchanged after oral L-arginine. Measures of oxidative stress and exercise performance after L-arginine/placebo were similar in placebo and active groups.
In men with stable angina, an increase in plasma L-arginine/ADMA ratio after two weeks' oral supplementation with L-arginine is not associated with an improvement in endothelium-dependent vasodilatation, oxidative stress or exercise performance.
本研究旨在确定L-精氨酸两周治疗对稳定型心绞痛男性患者血浆L-精氨酸与不对称二甲基精氨酸（ADMA）比值、氧化应激、乙酰胆碱介导的内皮依赖性血管舒张、运动能力及心率变异性的影响。
血浆L-精氨酸与ADMA的比值被认为是内皮依赖性舒张功能的决定因素；在某些情况下，补充L-精氨酸已被证明可改善内皮依赖性血管舒张及症状。
40例稳定型心绞痛男性患者，至少有一支心外膜冠状动脉狭窄>50%且运动试验阳性，按照双盲平行组设计随机分为两组，分别接受L-精氨酸（每日15 g）或安慰剂治疗两周。检测血浆L-精氨酸、ADMA、8-表-前列腺素F2α（氧化应激标志物）以及前臂血管对肱动脉输注硝普钠和乙酰胆碱（±L-精氨酸）的舒张反应。在治疗期开始和结束时进行标准的Bruce方案运动试验。
口服L-精氨酸后血浆L-精氨酸升高，而ADMA保持不变，导致L-精氨酸/ADMA比值增加62±11%（平均值±标准误，p<0.01）。尽管在基线时动脉内注射L-精氨酸可显著增强乙酰胆碱反应，但口服L-精氨酸后该反应未发生变化。安慰剂组和治疗组在接受L-精氨酸/安慰剂治疗后的氧化应激和运动能力指标相似。
在稳定型心绞痛男性患者中，口服L-精氨酸两周后血浆L-精氨酸/ADMA比值升高与内皮依赖性血管舒张、氧化应激或运动能力的改善无关。
