Vatner S F, Hintze T H, Macho P
Circ Res. 1982 Jul;51(1):56-66. doi: 10.1161/01.res.51.1.56.
We examined, in conscious dogs, the effects of beta-adrenergic stimulation on measurements of left circumflex coronary arterial diameter and blood flow and on calculations of late diastolic coronary resistance (LDCR) and left circumflex coronary internal cross-sectional area (CSA). Isoproterenol (0.1 microgram/kg) initially decreased mean arterial pressure by 25 +/- 2% (mean +/- SEM), and LDCR by 62 +/- 4%, and increased heart rate by 82 +/- 10%, left ventricular (LV) dP/dt by 79 +/- 12%, and mean coronary blood flow by 85 +/- 5%, while CSA rose slightly. The peak effects on CSA (24 +/- 2%) occurred later, along with decreases in mean arterial pressure (7.4 +/- 1.0%) and LDCR (25 +/-5.3%) and increases in coronary blood flow (14 +/- 2%), LV dP/dt (12 +/- 3%), and heart rate (24 +/- 4%). Pirbuterol (1.0 microgram/kg) induced changes that were qualitatively similar to those induced by isoproterenol. Prenalterol (20 micrograms/kg), a cardioselective beta 1-adrenergic receptor agonist, did not affect mean arterial pressure, but increased heart rate by 40 +/- 5%, LV dP/dt by 72 +/- 10%, mean coronary blood flow by 34 +/- 11%, and CSA by 26 +/- 3%, and decreased LDCR by 29 +/- 5+. Isoproterenol and pirbuterol, but not prenalterol, increased coronary sinus O2 content and decreased A-VO2 difference. After beta 1-adrenergic receptor blockade with atenolol (1 mg/kg), prenalterol no longer induced significant effects, whereas isoproterenol and pirbuterol decreased mean arterial pressure similarly to what was observed prior to blockade, but did not increase LV dP/dt, and induced attenuated increases in mean coronary blood flow, CSA, and decreases in LDCR. Thus, in the intact, conscious animal, large coronary arteries are regulated by beta-adrenergic mechanisms. Surprisingly, a major fraction of large coronary arterial dilation appeared to be either directly or indirectly due to beta 1-adrenergic receptor mechanisms, although beta 2-adrenergic effects were also significant.
我们在清醒犬中研究了β-肾上腺素能刺激对左旋冠状动脉直径、血流量的测量以及舒张末期冠状动脉阻力(LDCR)和左旋冠状动脉内横截面积(CSA)计算结果的影响。异丙肾上腺素(0.1微克/千克)最初使平均动脉压降低25±2%(平均值±标准误),使LDCR降低62±4%,使心率增加82±10%,使左心室(LV)dP/dt增加79±12%,使平均冠状动脉血流量增加85±5%,而CSA略有上升。对CSA的峰值效应(24±2%)出现较晚,同时平均动脉压降低(7.4±1.0%),LDCR降低(25±5.3%),冠状动脉血流量增加(14±2%),LV dP/dt增加(12±3%),心率增加(24±4%)。吡布特罗(1.0微克/千克)引起的变化在性质上与异丙肾上腺素引起的变化相似。普瑞特罗(20微克/千克),一种心脏选择性β1-肾上腺素能受体激动剂,不影响平均动脉压,但使心率增加40±5%,LV dP/dt增加72±10%,平均冠状动脉血流量增加34±11%,CSA增加26±3%,并使LDCR降低29±5%。异丙肾上腺素和吡布特罗,但不是普瑞特罗,增加了冠状窦O2含量并降低了动静脉氧差。在用阿替洛尔(1毫克/千克)进行β1-肾上腺素能受体阻断后,普瑞特罗不再产生显著影响,而异丙肾上腺素和吡布特罗使平均动脉压降低的程度与阻断前观察到的相似,但不增加LV dP/dt,并使平均冠状动脉血流量、CSA的增加减弱,使LDCR的降低减弱。因此,在完整的清醒动物中,大冠状动脉受β-肾上腺素能机制调节。令人惊讶的是,尽管β2-肾上腺素能效应也很显著,但大冠状动脉扩张的很大一部分似乎直接或间接归因于β1-肾上腺素能受体机制。