Müller P, Czernin J, Choi Y, Aguilar F, Nitzsche E U, Buxton D B, Sun K, Phelps M E, Huang S C, Schelbert H R
Department of Radiological Sciences, School of Medicine, University of California, Los Angeles.
Am Heart J. 1994 Jul;128(1):52-60. doi: 10.1016/0002-8703(94)90009-4.
Physical stress might modulate myocardial blood flow in near-maximally dilated coronary arteries by increasing coronary perfusion pressure, myocardial contractility, and heart rate. The net effect of these changes on hyperemic blood flows has not yet been defined in humans. To quantify the effect of physical exercise on pharmacologically induced hyperemia, myocardial blood flow was measured in 11 healthy volunteers. Measurements were performed with positron emission tomographic imaging with nitrogen-13 ammonia at rest, during intravenous (i.v.) adenosine administration (140 micrograms.kg-1.min-1 over 6 minutes), and during i.v. adenosine administration plus supine bicycle exercise with a maximal workload of 125 W. Myocardial blood flow was quantified by using a previously validated graphic analysis. Heart rate, systolic blood pressure, rate-pressure product, and mean aortic blood pressures were significantly higher during combined physical and pharmacologic stress than during pharmacologic stress alone. However, myocardial blood flow decreased from 2.6 +/- 0.4 to 2.2 +/- 0.4 ml.min-1.gm-1 with the addition of physical stress (p < 0.05). This decline was associated with a significant increase in coronary vascular resistance (35 +/- 6 vs 52 +/- 13 mm Hg.ml-1.gm.min; p < 0.05). Accordingly, myocardial flow reserve declined, from 5.0 +/- 0.9 to 4.3 +/- 1.0, with exercise supplementation (p < 0.05). Exercise in addition to pharmacologic stress increases coronary vascular resistance and thus significantly decreases hyperemic myocardial blood flow and flow reserve. This decrease results most likely from an increase in extravascular restrictive forces caused by higher ventricular pressures and contractility during physical stress.
体力应激可能通过增加冠状动脉灌注压、心肌收缩力和心率来调节接近最大扩张状态的冠状动脉中的心肌血流。这些变化对充血性血流的净效应在人类中尚未明确。为了量化体育锻炼对药物诱导的充血的影响，对11名健康志愿者的心肌血流进行了测量。测量在静息状态、静脉注射腺苷（6分钟内140微克·千克⁻¹·分钟⁻¹）期间以及静脉注射腺苷加仰卧位自行车运动（最大负荷125瓦）期间，使用氮-13氨正电子发射断层成像进行。通过使用先前验证的图形分析对心肌血流进行量化。与单独药物应激相比，体力和药物联合应激期间心率、收缩压、心率-血压乘积和平均主动脉血压显著更高。然而，加入体力应激后，心肌血流从2.6±0.4降至2.2±0.4毫升·分钟⁻¹·克⁻¹（p<0.05）。这种下降与冠状动脉血管阻力显著增加相关（35±6对52±13毫米汞柱·毫升⁻¹·克·分钟；p<0.05）。因此，运动补充后心肌血流储备从5.0±0.9降至4.3±1.0（p<0.05）。除药物应激外进行运动可增加冠状动脉血管阻力，从而显著降低充血性心肌血流和血流储备。这种降低最可能是由于体力应激期间心室压力和收缩力增加导致血管外限制性力量增加所致。
