Ferlito S, Gallina M
Chair of Semeiology and Medical Methodology, Garibaldi Hospital, Catania, Italy.
Minerva Cardioangiol. 1997 Nov;45(11):553-8.
The authors carried out a study on the plasmatic levels of nitrites, which are the sole stable metabolites of nitric oxide (NO), in a group of subjects suffering from various clinical forms of coronary artery disease, aimed at evaluating the endothelial production of NO in acute and chronic ischemic conditions.
Our series consisted of 104 female subjects (mean age 65 +/- 5) subdivided into: a) 10 subjects with acute coronary heart disease (myocardial infarction); b) 32 with chronic non hypertensive coronary heart disease (CHD); c) 30 with hypertensive CHD (arterial blood pressure over 160/95 mmHg); d) 32 with CHD and hypercholesterolemia (values over 250 mg/dl). Thirty-seven female subjects (mean age 58 +/- 7) without internistic diseases were considered as control subjects. For each sample the plasmatic levels of nitrites were determined by the Gutman and Hollywood method.
We discovered that in the patients with chronic coronary heart disease (CHD) the mean value of nitrites was 18 +/- 0.3 mumol/L, not significantly different from the controls (17 +/- 0.5 mumol/L). In the patients with acute CHD the nitrite plasma level were significantly (p < 0.05) higher (30 +/- 2.2 mumol/L) compared to the controls and the patients with chronic CHD. In the group of patients with hypertensive CHD the mean nitrite value was 20 +/- 0.6 mumol/L, significantly (p < 0.05) higher in comparison with the group of non-hypertensive CHD patients (14 +/- 0.3 mumol/L). In the subjects with CHD and hypercholesterolemia the mean value of nitrites was sharply elevated, (25 +/- 1.0 mumol/L), with a highly significant difference (p < 0.01) as compared to the normolipemic CHD patients.
These results lead to the hypothesis that: strong NO production may play a compensatory and protective role during acute myocardial hypoxia; NO defective synthesis may depend on an exhaustive endothelial adjustment in subjects with long-term CHD; a significant increase of the relaxing factor in hypertensive conditions exists; a highly enhanced synthesis of the plasmatic nitrites in hypercholesterolemic patients means an engagement of NO to neutralize the endothelium-damaging molecular substances and particularly the oxided LDL.
作者对一组患有各种临床形式冠状动脉疾病的受试者的血浆亚硝酸盐水平进行了研究，亚硝酸盐是一氧化氮（NO）唯一稳定的代谢产物，旨在评估急性和慢性缺血状态下内皮细胞产生NO的情况。
我们的研究对象包括104名女性受试者（平均年龄65±5岁），分为：a）10名急性冠心病（心肌梗死）患者；b）32名慢性非高血压冠心病（CHD）患者；c）30名高血压冠心病患者（动脉血压超过160/95 mmHg）；d）32名冠心病合并高胆固醇血症患者（数值超过250 mg/dl）。37名无内科疾病的女性受试者（平均年龄58±7岁）作为对照。对每个样本采用古特曼和霍利迪方法测定血浆亚硝酸盐水平。
我们发现，慢性冠心病（CHD）患者亚硝酸盐的平均值为18±0.3 μmol/L，与对照组（17±0.5 μmol/L）无显著差异。急性冠心病患者的血浆亚硝酸盐水平显著高于对照组和慢性冠心病患者（30±2.2 μmol/L，p<0.05）。高血压冠心病患者组亚硝酸盐平均值为20±0.6 μmol/L，与非高血压冠心病患者组（14±0.3 μmol/L）相比显著升高（p<0.05）。冠心病合并高胆固醇血症患者亚硝酸盐平均值急剧升高（25±1.0 μmol/L），与血脂正常的冠心病患者相比差异极显著（p<0.01）。
这些结果得出以下假设：在急性心肌缺氧期间，大量产生NO可能起到代偿和保护作用；长期冠心病患者中，NO合成缺陷可能取决于内皮细胞的过度调节；高血压状态下存在舒张因子的显著增加；高胆固醇血症患者血浆亚硝酸盐的高度增强合成意味着NO参与中和损伤内皮的分子物质，尤其是氧化型低密度脂蛋白。
