Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone.
Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone.
复制标题
动脉粥样硬化性冠状动脉疾病患者吸烟引起的冠状血管收缩：肾上腺素介导的冠状动脉张力改变的证据。
DOI：
10.1161/01.cir.73.4.662
复制
发表时间：
1986
期刊：
影响因子：
37.8
通讯作者：
Hillis,LD
中科院分区：
文献类型：
--
作者：
Winniford,MD;Wheelan,KR;Kremers,MS;Ugolini,V;vandenBergJr,E;Niggemann,EH;Jansen,DE;Hillis,LD
在患有冠状动脉粥样硬化性疾病的患者中，吸烟增加心肌需氧量，但可能导致冠状动脉血流量和心肌氧供应的不适当减少。本研究旨在探讨吸烟诱导的冠状动脉血管收缩的机制，特别是确定吸烟是否会导致α-肾上腺素介导的冠状动脉张力增加。在36名患有冠心病的慢性吸烟者中（27名男性和9名女性，50 +/- 9 [平均值+/- SD]岁），心率-收缩期动脉压双乘积和冠状窦血流量（热稀释法）测定吸烟前后（1）生理盐水（n = 5，对照受试者），（2）α-肾上腺素能阻断剂酚妥拉明，5 mg（n = 15），（3）β-肾上腺素能阻断剂普萘洛尔，0.1 mg/kg（n = 12），或（4）硝普钠，0.4 - 0.8 μ g/kg/min，剂量足以使动脉收缩压降低15%（n = 4）。在初始吸烟期间，所有组的心率-血压乘积增加，冠状窦血流量未因吸烟而改变。30至75分钟后，给予生理盐水、酚妥拉明、普萘洛尔或硝普钠，并重复测量。在对照组中，心率-血压乘积和冠状窦血流量的反应与先前观察到的相似。在那些接受酚妥拉明的患者中，心率-血压乘积没有变化，但冠状窦血流量随着吸烟而显著增加（在第一次吸烟期间[酚妥拉明之前]的百分比变化为+2 +/-15%，在第二次吸烟期间[酚妥拉明之后]的百分比变化为+32 +/-17%; p <0.01）。（250字处删节）
In patients with atherosclerotic coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate decrease in coronary blood flow and myocardial oxygen supply. This study was performed to explore the mechanism of smoking-induced coronary vasoconstriction and, specifically, to determine if smoking causes an alpha-adrenergically mediated increase in coronary artery tone. In 36 chronic smokers with coronary artery disease (27 men and nine women, 50 +/- 9 [mean +/- SD] years old), heart rate-systolic arterial pressure double product and coronary sinus blood flow (by thermodilution) were measured before and during smoking both before and after (1) normal saline (n = 5, control subjects), (2) an alpha-adrenergic-blocking agent, phentolamine, 5 mg (n = 15), (3) a beta-adrenergic-blocking agent, propranolol, 0.1 mg/kg (n = 12), or (4) sodium nitroprusside, 0.4 to 0.8 micrograms/kg/min, given in a dose sufficient to diminish systolic arterial pressure by 15% (n = 4). During the initial smoking period, rate-pressure product increased and coronary sinus blood flow was unchanged by smoking in all groups. After 30 to 75 min, saline, phentolamine, propranolol, or sodium nitroprusside was given, and measurements were repeated. In the control subjects, rate-pressure product and coronary sinus blood flow responded in a similar manner to that observed previously. In those receiving phentolamine, rate-pressure product was unchanged, but coronary sinus blood flow rose substantially with smoking (percent change +2 +/- 15% during the first smoking period [before phentolamine] and +32 +/- 17% during the second smoking period [after phentolamine]; p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)