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目的观察吸烟对血管内应依赖性舒张功能的影响，探讨吸烟对心血管危害的机制。方法采用 Ｃｅｌｅｒｍａｊｅｒ的方法，对ｓｌ例吸烟者和３５例正常对照者，分别在静息时、反应性充血后、舌下含硝酸甘油后测定肽动脉口径。测定各组受试者试验前后血浆ＮＯ、ＥＴ、ＰＧＩ；、ＴｘＢ；浓度。结果肽动脉ＦＭＤ（ｎｏｗ－ｍｅｄｉａｔｅｄ ｄｉｌａｔａｔｉｏｎ，内皮依赖性舒张），正常组明显高于吸烟组，分别为（１０．１２％，８．２４％，７．１５％，６．１４％，４．０２％），血浆ＮＯ、ＰＧＩ；正常组明显高于吸烟组，而血浆ＥＴ、ＴＸＢ；正常组明显低于吸烟组。结论香烟的毒性成分能直接损害血管内皮细胞，导致内皮功能失调。吸烟引起血管内皮舒张功能障碍可能与ＮＯ、ＰＧＩ；减少，内皮素、ＴＸＢ２增多致血管异常收缩有关。
Objective To observe the effect of smoking on endothelium-dependent diastolic function and to explore the mechanism of smoking on cardiovascular risk. Methods The Celermajer method was used to measure the diameter of arterioles in patients with sl smokers and 35 normal controls at rest and after reactive hyperemia with sublingual nitroglycerin. Plasma NO, ET, PGI; and TxB concentrations were measured before and after the test in each group. Results Now-mediated dilatation (FMD) was significantly higher in the normal group than in the smoking group (10.12%, 8.24%, 7.15%, 6.14%, 4.02 %), Plasma NO, PGI; the normal group was significantly higher than the smoking group, while the plasma ET, TXB; normal group was significantly lower than the smoking group. Conclusion Toxic components of cigarettes can directly damage vascular endothelial cells, leading to endothelial dysfunction. Smoking caused by vascular endothelial dysfunction may be NO, PGI; reduce endothelin, TXB2 increased vascular abnormal contraction.