Laxson D D, Homans D C, Dai X Z, Sublett E, Bache R J
Department of Medicine, University of Minnesota Medical School, Minneapolis.
Circ Res. 1989 Jan;64(1):9-20. doi: 10.1161/01.res.64.1.9.
Coronary vascular responses in regions of reversible postischemic myocardial contractile dysfunction (stunned myocardium) were examined in chronically instrumented, awake dogs. Left anterior descending coronary artery blood flow and oxygen extraction, aortic and left ventricular pressures, and regional myocardial segment shortening were determined. Regional myocardial blood flow was measured with microspheres. Coronary reactive hyperemia and vasodilator reserve, and regional myocardial oxygen consumption were determined. Three sequential 10-minute left anterior descending coronary artery occlusions separated by 30-minute reperfusion periods resulted in progressive postischemic dysfunction so that 1 hour after the final coronary artery occlusion, myocardial segment shortening was reduced to 37% of baseline. Despite this decrease in contractile function, left anterior descending artery flow (19.6 +/- 2.6 vs. 18.4 +/- 3.0 ml/min), myocardial blood flow and the transmural distribution of flow measured with microspheres, and regional myocardial oxygen consumption were unchanged. Although the coronary vasodilator reserve in response to adenosine was unaltered (63 +/- 9 vs. 70 +/- 15 ml/min), the reactive hyperemia response to a 10-second coronary occlusion was decreased in intensity (debt repayment ratio = 474 +/- 78% vs. 322 +/- 74%; p less than 0.05) and duration (57 +/- 9.1 vs. 35 +/- 4.5 seconds; p less than 0.05), while the peak flow response was unchanged (57 +/- 6.8 vs. 60 +/- 7.1 ml/min). Thus, in the intact awake animal postischemic myocardial contractile dysfunction was not associated with decreased myocardial oxygen consumption and did not impair the normal relation between coronary blood flow and myocardial oxygen utilization. Although coronary vessels showed a normal ability to vasodilate in response to adenosine, coronary reactive hyperemia was reduced.
在长期植入仪器的清醒犬中，研究了可逆性缺血后心肌收缩功能障碍（顿抑心肌）区域的冠状血管反应。测定了左前降支冠状动脉血流量和氧摄取、主动脉和左心室压力以及局部心肌节段缩短情况。用微球测量局部心肌血流量。测定了冠状动脉反应性充血和血管舒张储备以及局部心肌氧耗。三次连续10分钟的左前降支冠状动脉闭塞，中间间隔30分钟的再灌注期，导致进行性缺血后功能障碍，因此在最后一次冠状动脉闭塞后1小时，心肌节段缩短减少至基线的37%。尽管收缩功能有所下降，但左前降支血流量（19.6±2.6对18.4±3.0 ml/min）、心肌血流量以及用微球测量的血流跨壁分布和局部心肌氧耗均未改变。虽然对腺苷的冠状动脉血管舒张储备未改变（63±9对70±15 ml/min），但对10秒冠状动脉闭塞的反应性充血反应强度降低（偿还率=474±78%对322±74%；p<0.05），持续时间缩短（57±9.1对35±4.5秒；p<0.05），而峰值血流反应未改变（57±6.8对60±7.1 ml/min）。因此，在完整的清醒动物中，缺血后心肌收缩功能障碍与心肌氧耗减少无关，也不损害冠状动脉血流与心肌氧利用之间的正常关系。虽然冠状动脉血管对腺苷有正常的舒张能力，但冠状动脉反应性充血减少。
