Carlson R E, Kavanaugh K M, Buda A J
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0366.
Am Heart J. 1988 Aug;116(2 Pt 1):536-45. doi: 10.1016/0002-8703(88)90629-1.
Myocardial ischemia may be produced by limitation of blood flow as in abrupt coronary occlusion, termed supply-type ischemia, or by increasing myocardial oxygen demand in the setting of restricted flow, termed demand-type ischemia. To examine the comparative extent and severity of the dysfunction related to both forms of ischemia, we studied anesthetized, open-chest dogs by means of two-dimensional echocardiography and tracer microspheres. Supply-type ischemia was produced by total occlusion of the LCx (n = 7); demand-type ischemia was induced by infusion of dobutamine after creation of a critical LCx stenosis (n = 6). At the time of the production of ischemia, the group with demand-type ischemia had significant increases in both heart rate (p less than 0.05) and mean arterial pressure (p less than 0.05), whereas the group with supply-type ischemia had a decrease in mean arterial pressure (p less than 0.05). Subendocardial blood flow in the LCx region was severely depressed in supply-type ischemia (0.09 +/- 0.04 ml/min/gm) compared to demand-type ischemia (1.04 +/- 0.07 ml/min/gm; p less than 0.01). Although both groups of animals had an abnormality of left ventricular function during ischemia, as determined by two-dimensional echocardiography, the extent of the dysfunction in the group with supply-type ischemia was greater (146 +/- 12 degrees) compared to the group with demand-type ischemia (99 +/- 9 degrees; p less than 0.01). Similarly, the degree of left ventricular dysfunction in the group with supply-type ischemia was greater than that for the group with demand-type ischemia (p less than 0.05). Thus these data suggest that supply-type ischemia produced by coronary occlusion results in a greater extent and degree of left ventricular functional abnormality than pharmacologically induced demand-type ischemia.
心肌缺血可能由血流受限引起，如冠状动脉突然闭塞，称为供应型缺血；或在血流受限的情况下，因心肌需氧量增加而导致，称为需求型缺血。为了研究与这两种缺血形式相关的功能障碍的相对程度和严重性，我们通过二维超声心动图和示踪微球对麻醉开胸犬进行了研究。供应型缺血通过左旋支动脉（LCx）完全闭塞产生（n = 7）；需求型缺血在造成LCx严重狭窄后通过静脉输注多巴酚丁胺诱发（n = 6）。在产生缺血时，需求型缺血组的心率（p < 0.05）和平均动脉压（p < 0.05）均显著升高，而供应型缺血组的平均动脉压降低（p < 0.05）。与需求型缺血（1.04 ± 0.07 ml/min/gm；p < 0.01）相比，供应型缺血时LCx区域的心内膜下血流严重降低（0.09 ± 0.04 ml/min/gm）。尽管两组动物在缺血期间通过二维超声心动图测定均存在左心室功能异常，但供应型缺血组的功能障碍程度（146 ± 12度）大于需求型缺血组（99 ± 9度；p < 0.01）。同样，供应型缺血组的左心室功能障碍程度大于需求型缺血组（p < 0.05）。因此，这些数据表明，冠状动脉闭塞产生的供应型缺血比药物诱导的需求型缺血导致更大程度和更高程度的左心室功能异常。
