Laxson D D, Dai X Z, Homans D C, Bache R J
Department of Medicine, University of Minnesota, Minneapolis 55455.
Circulation. 1992 Jan;85(1):313-22. doi: 10.1161/01.cir.85.1.313.
Previous work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoperfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise.
Studies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary artery perfusion pressure to approximately 40 mm Hg. Measurements of myocardial blood flow were made with radioactive microspheres during exercise (6.5 km/hr, 6% grade) before and during intracoronary infusion of the potent coronary vasodilator adenosine (40 micrograms/kg/min). Distal coronary perfusion pressure was held equal before and during intracoronary adenosine infusion (43 +/- 5 versus 42 +/- 5 mm Hg) by adjusting the hydraulic coronary occluder. During exercise in the presence of a coronary stenosis, myocardial blood flow (milliliter per minute per gram) was significantly reduced in all layers of the ischemic posterior region compared with the nonischemic anterior region. During intracoronary adenosine infusion, with no change in coronary perfusion pressure, myocardial blood flow was significantly increased compared with preadenosine flows for both the subendocardial layer flow (1.03 +/- 0.74 versus 0.66 +/- 0.50; p less than 0.05) and mean transmural flow (1.54 +/- 0.59 versus 1.16 +/- 0.36; p less than 0.05). In the presence of a coronary stenosis, regional myocardial segment shortening in the ischemic region during exercise fell significantly to 49 +/- 8% of shortening in the absence of a coronary stenosis but improved modestly during adenosine infusion (65 +/- 7 versus 49 +/- 8%; p less than 0.05).
These results indicate that adenosine-responsive coronary vasodilator reserve persists during exercise-induced myocardial ischemia and suggest that residual microvascular vasoconstrictor tone may affect the extent of myocardial hypoperfusion occurring consequent to a flow-limiting coronary stenosis.
先前的研究报道，在因灌注不足而导致缺血的心肌中，冠状血管扩张储备可能持续存在。本研究调查了在运动期间因限流性冠状动脉狭窄而急性缺血的心肌区域中残余冠状血管运动张力的存在情况及程度。
对长期植入仪器的犬进行研究，这些犬在存在冠状动脉狭窄的情况下进行跑步机运动，该狭窄使左回旋支冠状动脉远端灌注压降至约40 mmHg。在运动期间（6.5 km/hr，6%坡度），在冠状动脉内注入强效冠状血管扩张剂腺苷（40微克/千克/分钟）之前和期间，用放射性微球测量心肌血流量。通过调节液压冠状动脉闭塞器，使冠状动脉内注入腺苷之前和期间的远端冠状动脉灌注压保持相等（43±5对42±5 mmHg）。在存在冠状动脉狭窄的运动期间，与非缺血的前壁区域相比，缺血后壁区域的所有层心肌血流量（每分钟每克毫升数）均显著降低。在冠状动脉内注入腺苷期间，冠状动脉灌注压无变化，与注入腺苷前相比，心内膜下层血流量（1.03±0.74对0.66±0.50；p<0.05）和平均透壁血流量（1.54±0.59对1.16±0.36；p<0.05）均显著增加。在存在冠状动脉狭窄的情况下，运动期间缺血区域的局部心肌节段缩短显著降至无冠状动脉狭窄时缩短的49±8%，但在注入腺苷期间有适度改善（65±7对49±8%；p<0.05）。
这些结果表明，腺苷反应性冠状血管扩张储备在运动诱导的心肌缺血期间持续存在，并提示残余微血管血管收缩张力可能影响因限流性冠状动脉狭窄而发生的心肌灌注不足的程度。
