EFFECTS OF REGIONAL ALPHA-BLOCKADE AND BETA-BLOCKADE ON RESTING AND HYPEREMIC CORONARY BLOOD-FLOW IN CONSCIOUS, UNSTRESSED HUMANS
EFFECTS OF REGIONAL ALPHA-BLOCKADE AND BETA-BLOCKADE ON RESTING AND HYPEREMIC CORONARY BLOOD-FLOW IN CONSCIOUS, UNSTRESSED HUMANS
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DOI：
10.1161/01.cir.79.4.797
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发表时间：
1989-04-01
期刊：
影响因子：
37.8
通讯作者：
THAMES, MD
中科院分区：
文献类型：
--
作者：
HODGSON, JM;COHEN, MD;THAMES, MD
我们的目的是确定是否有基础肾上腺素能对人体冠状动脉循环的影响。我们研究了56例心脏移植后失神经支配的心脏患者和19例冠状动脉造影正常的正常神经支配患者。在心导管检查过程中，使用3F冠状动脉内多普勒导管测量冠状动脉血流速度。通过心房起搏控制心率。心外膜冠状动脉直径通过数字冠状动脉造影照片的自动分析来测量。冠状动脉内注射盐酸罂粟碱（12 mg）评估冠状动脉血流储备。通过冠状动脉内注射酚妥拉明（3 mg，α）和普萘洛尔（2 mg，β.）或美托洛尔（3 mg，β 1）。在α之后-阻断后，平均动脉压在去神经移植（-5.8 . ±. 1.5%）（平均值±）。SEM）和正常神经支配的患者（-12.6 . ±-. 3.2%）。在这些组中也观察到冠状动脉血流速度降低（-8.2 . ±-. 2.3%和-9.2 . ±-. 5.8%）。计算出的冠状血管阻力没有变化。当患者用β-IFN-γ预治疗时，观察到类似的变化。在α-之前封锁封锁非特异性β-阻断不影响平均动脉压，但降低冠状动脉速度（神经支配，-11.6 . ±-.失神经支配组为-9.3 . ±-. 2.4%）和增加的冠状动脉血管阻力（神经支配25.4 . ±. 6.7%;去神经10.2 . ±. 3.7%）。在用美托洛尔选择性阻断β 1后，两组的冠状血管阻力均未升高。在任一α-β治疗后，任一患者组的冠状动脉血流储备均未改变。或β-封锁心外膜冠状动脉直径的变化很小，通常不显著。这些数据表明，α-受体介导的血管张力在去神经移植患者和正常神经支配的患者中都是可以忽略的。此外，在非选择性β-受体阻滞剂治疗后血管阻力的增加也是可能的。阻断是直接β 2血管作用的结果。我们的数据进一步表明，有很少的肾上腺素介导的心外膜动脉张力（无论是体液或神经）在休息和最大的血管扩张反应不受肾上腺素介导的血管紧张素。
Our purpose was to determine if there are basal adrenergic influences on the coronary circulation in humans. We studied 56 patients with denervated hearts after cardiac transplantation and 19 normally innervated patients with angiographically normal coronary arteries. Coronary blood flow velocity was measured during cardiac catheterization with a subselective 3F intracoronary Doppler catheter. Heart rate was controlled by atrial pacing. Epicardial coronary artery diameter was measured by automated analyses of digital coronary angiograms. Coronary flow reserve was assessed by intracoronary papaverine hydrochloride (12 mg) injections. Regional sympathetic blockade was produced by intracoronary injections of phentolamine (3 mg, .alpha.) and propranolol (2 mg, .beta.) or metoprolol (3 mg, .beta.1). After .alpha.-blockade, mean arterial pressure fell significantly (p < 0.05) in both the denervated transplant (-5.8 .+-. 1.5%) (mean .+-. SEM) and normally innervated patients (-12.6 .+-. 3.2%). Reductions in coronary flow velocity also were observed in these groups (-8.2 .+-. 2.3% and -9.2 .+-. 5.8%, respectively). Calculated coronary vascular resistance was unchanged. Similar changes were seen when patients were pretreated with .beta.-blockade before .alpha.-blockade. Nonspecific .beta.-blockade did not affect mean arterial pressure but decreased coronary velocity (innervated, -11.6 .+-. 3.9%; denervated, -9.3 .+-. 2.4%) and increased coronary vascular resistance (innervated 25.4 .+-. 6.7%; denervated 10.2 .+-. 3.7%). Coronary vascular resistance did not rise in either group after selective .beta.1-blockade with metoprolol. Coronary flow reserve did not change in either patient group after either .alpha.- or .beta.-blockade. Changes in epicardial coronary artery diameter were small and generally not significant. These data suggest that .alpha.-receptor-mediated vascular tone is negligible in both denervated transplant patients and normally innervated patients. Additionally, the increase in vascular resistance after nonselective .beta.-blockade is the result of direct .beta.2 vascular effects. Our data further suggest that there is little adrenergically mediated epicardial artery tone (either humoral or neural) at rest and that maximal vasodilator responses are not limited by adrenergically mediated vasomotor tone.