冠心病患者急性运动对一氧化氮的反应

A. Kaya, Alev Arat-Özkan, Özge Köner, H. Balcı, O. Abacı, T. Gürmen, S. Kucukoğlu, Z. Yiğit
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摘要

一氧化氮(NO)已被确定为一种从内皮细胞释放的血管舒张物质,在动脉粥样硬化存在时减少。本研究旨在评估未经训练的糖尿病和非糖尿病合并动脉粥样硬化性冠状动脉疾病(CAD)患者急性运动时的全身NO反应。这是一项前瞻性临床研究,由三组组成。A组(n=50)为非糖尿病性CAD患者,B组(n=20)为糖尿病、CAD患者,C组(n=20)为健康对照。所有患者在24小时低亚硝酸盐/硝酸盐饮食后,根据改良布鲁斯方案进行标准症状限制跑步机运动试验。由于一氧化氮的半衰期很短,因此测定了一氧化氮代谢(NOx)的最终产物。糖尿病患者(24±8.4μmol/L,p<0.0001)和非糖尿病患者(43.5±13.7μmol/L, p<0.01)的基础血清NOx水平均显著低于对照组(66.5±3.4μmol/L)。只有在非糖尿病、冠心病患者组中,通过运动观察到NOx水平升高。在糖尿病患者中,运动未观察到氮氧化物含量增加。CAD患者组或对照组。在正常对照中,运动没有引起氮氧化物水平的显著变化。运动诱导的动脉粥样硬化性疾病患者全身氮氧化物水平的增加可能表明一种代偿机制,这种机制在糖尿病亚组中不存在或减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nitric Oxide Response to Acute Exercise in Patients with Coronary Artery Disease
Nitric oxide (NO) has been identified as a vasodilatory substance released from the endothelium which decreases in the presence of atherosclerosis. This study aimed to evaluate the systemic NO response to acute exercise in untrained diabetic and nondiabetic patients with atherosclerotic coronary artery disease (CAD). This is a prospective, clinical study consisting of three groups. Group A (n=50) consisted of nondiabetic CAD patients,group B (n=20) consisting of diabetic, CAD patients and group C (n=20) of healthy controls. All patients underwent a standard symptom limited treadmill exercise test according to the modified Bruce protocol after 24 hours low nitrite/ nitrate diet. End products of nitric oxide metabolism (NOx) were determined as the half life of NO is very short. Basal serum NOx levels of both diabetics (24±8.4μmol/L,p<0.0001)and nondiabetics (43.5±13.7μmol/L, p<0.01) were significantly lower compared to controls (66.5±3.4μmol/L). Only in the nondiabetic, CAD patient group was an increase in NOx levels observed with exercise. No increase in NOx with exercise was observed for the diabetic. CAD patient group or for the control group. In normal controls exercise induced no significant change in NOx levels. Exercise induced increase in systemic NOx levels in patients with atherosclerotic disease may indicate a compensatory mechanism which is not present or diminished in the diabetic subgroup .
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