Montes de Oca Maria, Loeb Eduardo, Torres Sonia H, De Sanctis Juan, Hernández Noelina, Tálamo Carlos
Pulmonary Division, Hospital Universitario de Caracas, Universidad Central de Venezuela, Los Chaguaramos, Caracas, Venezuela.
Chest. 2008 Jan;133(1):13-8. doi: 10.1378/chest.07-1592.
Although tobacco smoke is the main cause of COPD, relatively little attention has been paid to its potential damage to skeletal muscle. This article addresses the effect of smoking on skeletal muscle.
The vastus lateralis muscle was studied in 14 non-COPD smokers (FEV(1)/FVC, 78 +/- 5%) and 20 healthy control subjects (FEV(1)/FVC, 80 +/- 3%). Muscular structure, enzyme activity, constitutive and inducible nitric oxide (NO) synthases (endothelial NO oxide synthase [eNOS], neuronal NO synthase [nNOS] and inducible NO synthase [iNOS]), nitrites, nitrates, nitrotyrosine, and the presence of macrophages were analyzed.
In smokers, type I muscle fibers cross-sectional area was decreased, and a similar trend was found in type IIa fibers. Lactate dehydrogenase levels and the percentage of fibers with low oxidative and high glycolytic capacity were increased in smokers. nNOS (96.9 +/- 11.7 vs 125.4 +/- 31.9 ng/mg protein; p < 0.01) and eNOS (38.9 +/- 11.0 vs 45.2 +/- 7.7 ng/mg protein [+/- SD]; p < 0.05) were lower in smokers, while fiber type distribution, capillarity measures, beta-hydroxy-acyl-CoA-dehydrogenase levels, iNOS, nitrite, nitrate, and nitrotyrosine levels, and macrophage number in the muscle tissue were similar to the nonsmoker subjects.
Smokers presented some alterations of skeletal muscle such as oxidative fiber atrophy, increased glycolytic capacity, and reduced expression of the constitutive NO synthases (eNOS and nNOS). The findings support some muscular structural and metabolic damage but not the presence of local inflammation in the smokers. In addition, they suggest a possible effect of tobacco smoke impairing the normal process of NO generation.
尽管烟草烟雾是慢性阻塞性肺疾病（COPD）的主要病因，但人们对其对骨骼肌的潜在损害关注相对较少。本文探讨吸烟对骨骼肌的影响。
对14名非COPD吸烟者（第一秒用力呼气容积/用力肺活量[FEV(1)/FVC]，78±5%）和20名健康对照者（FEV(1)/FVC，80±3%）的股外侧肌进行研究。分析肌肉结构、酶活性、组成型和诱导型一氧化氮（NO）合酶（内皮型NO合酶[eNOS]、神经元型NO合酶[nNOS]和诱导型NO合酶[iNOS]）、亚硝酸盐、硝酸盐、硝基酪氨酸以及巨噬细胞的存在情况。
吸烟者中，I型肌纤维横截面积减小，IIa型纤维也有类似趋势。吸烟者的乳酸脱氢酶水平以及低氧化和高糖酵解能力纤维的百分比增加。吸烟者的nNOS（96.9±11.7对125.4±31.9 ng/mg蛋白质；p<0.01）和eNOS（38.9±11.0对45.2±7.7 ng/mg蛋白质[±标准差]；p<0.05）较低，而肌肉组织中的纤维类型分布、毛细血管指标、β-羟基酰基辅酶A脱氢酶水平、iNOS、亚硝酸盐、硝酸盐和硝基酪氨酸水平以及巨噬细胞数量与非吸烟者相似。
吸烟者存在一些骨骼肌改变，如氧化型纤维萎缩、糖酵解能力增加以及组成型NO合酶（eNOS和nNOS）表达降低。这些发现支持吸烟者存在一些肌肉结构和代谢损伤，但不存在局部炎症。此外，它们提示烟草烟雾可能影响NO生成的正常过程。
