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首页> 外文期刊>American Journal of Physiology >Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries.
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Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries.

机译：吸烟对小鼠动脉一氧化氮，结构和机械特性的影响。

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Cigarette smoking (CS) is a major risk factor for vascular disease. The aim of this study was to quantitatively assess the influence of CS on mouse arteries. We studied the effect of short-term (6 wk) and long-term (16 wk) CS exposure on structural and mechanical properties of coronary arteries compared with that of control mice. We also examined the reversibility of the deleterious effects of CS on structural [e.g., wall thickness (WT)], mechanical (e.g., stiffness), and biochemical [e.g., nitric oxide (NO) by-products] properties with the cessation of CS. The left and right coronary arteries were cannulated in situ and mechanically distended. The stress, strain, elastic modulus, and WT of coronary arteries were determined. Western blot analysis was used to analyze endothelial NO synthase (eNOS) in the femoral and carotid arteries of the same mice, and NO by-products were determined by measuring the levels of nitrite. Our results show that the mean arterial pressure was increased by CS. Furthermore, CS significantly increased the elastic modulus, decreased stress and strain, and increased the WT and WT-to-radius ratio compared with those of control mice. The reduction of eNOS protein expression was found only after long-term CS exposure. Moreover, the NO metabolite was markedly decreased in CS mice after short- and long-term exposure of CS. These findings suggest that 16 wk of CS exposure can cause an irreversible deterioration of structural and elastic properties of mouse coronary arteries. The decrease in endothelium-derived NO in CS mice was seen to significantly correlate with the remodeling of arterial wall.
机译：吸烟（CS）是血管疾病的主要危险因素。这项研究的目的是定量评估CS对小鼠动脉的影响。与对照小鼠相比，我们研究了短期（6周）和长期（16周）CS暴露对冠状动脉结构和机械特性的影响。我们还研究了CS停止后CS对结构[例如壁厚（WT）]，机械（例如刚度）和生化[例如一氧化氮（NO）副产物]有害作用的可逆性。 。左和右冠状动脉原位插管并机械扩张。确定了冠状动脉的应力，应变，弹性模量和WT。使用蛋白质印迹分析来分析同一只小鼠的股动脉和颈动脉中的内皮一氧化氮合酶（eNOS），并通过测量亚硝酸盐水平来确定一氧化氮的副产物。我们的结果表明，平均动脉压由CS增加。此外，与对照组相比，CS显着增加了弹性模量，降低了应力和应变，并增加了WT和WT半径。仅在长期接触CS后发现eNOS蛋白表达降低。此外，短期和长期接触CS后，CS小鼠的NO代谢产物明显减少。这些发现表明16周的CS暴露可导致小鼠冠状动脉的结构和弹性特性不可逆转地下降。观察到CS小鼠内皮源性NO的减少与动脉壁的重塑显着相关。

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