Kiowski W, Linder L, Stoschitzky K, Pfisterer M, Burckhardt D, Burkart F, Bühler F R
Division of Cardiology, University Hospital of Zürich, Switzerland.
Circulation. 1994 Jul;90(1):27-34. doi: 10.1161/01.cir.90.1.27.
Smoking is a major risk factor for the development of atherosclerosis. Because endothelial dysfunction may be a marker for future atherosclerosis, we investigated the effects of smoking on endothelium-dependent control of vascular tone.
The effects of brachial arterial infusions of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthesis inhibitor; sodium nitroprusside; endothelin-1; and norepinephrine on forearm blood flow (strain-gauge plethysmography) were compared in 29 long-term smokers and 16 nonsmokers. The acute effects of smoking on systemic hemodynamics, plasma catecholamines, and forearm vascular responses to these compounds were investigated in smokers only. Smokers did not differ from nonsmokers (n = 16) regarding the vascular effects of sodium nitroprusside (n = 13) or vasoconstriction due to norepinephrine and endothelin-1 (n = 16). Low-dose endothelin-1-induced vasodilation, believed to reflect endothelial prostacyclin or nitric oxide release, was absent in smokers (n = 16), and their increase of forearm vascular resistance (FVR) after L-NMMA (n = 13) was impaired (35.6 +/- 27.9% versus 118.8 +/- 43.2%, P < .001). Short-term smoking (n = 11) increased blood pressure, heart rate, and plasma epinephrine concentrations (P < .05 or less); enhanced endothelin-1-induced vasoconstriction (delta FVR, 457 +/- 192% versus 254 +/- 143%, P < .01); and decreased norepinephrine-induced vasoconstriction (P < .05), but had no effect on the other interventions.
Long-term smoking is associated with a diminished nitric oxide-dependent component of basal vascular tone and an impaired endothelium-dependent vasodilator response to low-dose endothelin-1 and short-term smoking enhances endothelin-1-induced vasoconstriction. Impaired endothelial control of vascular tone might reflect impairment of normal antiatherosclerotic endothelial functions in smokers, but the relevance of smoking-induced enhancement of endothelin-1 vasoconstriction remains to be determined.
吸烟是动脉粥样硬化发生的主要危险因素。由于内皮功能障碍可能是未来动脉粥样硬化的一个标志，我们研究了吸烟对血管张力的内皮依赖性调控的影响。
比较了29名长期吸烟者和16名不吸烟者肱动脉输注一氧化氮合成抑制剂NG-单甲基-L-精氨酸（L-NMMA）、硝普钠、内皮素-1和去甲肾上腺素对前臂血流量（应变片体积描记法）的影响。仅在吸烟者中研究了吸烟对全身血流动力学、血浆儿茶酚胺以及前臂血管对这些化合物反应的急性影响。吸烟者与不吸烟者（n = 16）在硝普钠（n = 13）的血管效应或去甲肾上腺素和内皮素-1引起的血管收缩（n = 16）方面没有差异。吸烟者（n = 16）不存在低剂量内皮素-1诱导的血管舒张，这种舒张被认为反映了内皮前列环素或一氧化氮的释放，并且他们在L-NMMA（n = 13）后前臂血管阻力（FVR）的增加受损（35.6±27.9%对118.8±43.2%，P <.001）。短期吸烟（n = 11）会升高血压、心率和血浆肾上腺素浓度（P <.05或更低）；增强内皮素-1诱导的血管收缩（ΔFVR，457±192%对254±143%，P <.01）；并降低去甲肾上腺素诱导的血管收缩（P <.05），但对其他干预措施没有影响。
长期吸烟与基础血管张力中一氧化氮依赖性成分的减少以及对低剂量内皮素-1的内皮依赖性血管舒张反应受损有关，短期吸烟会增强内皮素-1诱导的血管收缩。内皮对血管张力的调控受损可能反映了吸烟者正常抗动脉粥样硬化内皮功能的损害，但吸烟诱导的内皮素-1血管收缩增强的相关性仍有待确定。
