Nienaber C, Gottwik M, Winkler B, Schaper W
Basic Res Cardiol. 1983 Mar-Apr;78(2):210-26. doi: 10.1007/BF01906674.
It is well known that coronary occlusions of short duration do not produce infarcts in the dog heart, but permanent occlusions always do. The aim of this paper was to investigate with quantitative direct measurements the determinants of infarct size within these two extremes. We measured left ventricular MV2, coronary and collateral blood flow and infarct size after occlusion times varying between 45 minutes and 24 hours. MVO2 was kept low in one group by establishing low heart rates with a synthetic opiate. In another group, MV2 was kept elevated by giving synthetic catecholamines (dobutamine) that stimulated contractility and heart rate. Under the described experimental conditions LV-coronary blood flow reflected the true demand for blood and oxygen. The ratio of collateral blood flow over coronary blood flow (both measured with tracer microspheres) was therefore a good approximation of the supply-demand ratio (SD). Since collateral flow was inhomogeneously distributed across the left ventricular wall, the SD-ratio showed similar variations. As the collateral blood flow increased with elapsed time after coronary occlusion, the SD-ratio improved. Since high LV-O2-demand increased coronary flow but exerted practically no influence on collateral flow, this situation influenced the SD-ratio in a negative way. Decreased O2-demand had the opposite effect. The SD-ratio is thus a valid expression of the relative and absolute blood flow deficit as influenced by the local and general O2-demand. We found significant and characteristic correlations between the SD-ratio and infarct which was only influenced by time. A blood flow deficit of 90% (i.e., collateral flow = 10% of required flow) produced a 50%-infarct (relative to the risk-region) with a 45-min occlusion but a 90%-infarct with occlusion times of 3 hrs and longer. If the perfusion deficit is only 0.5 (collateral flow = 50% of required flow), no infarct is detectable at occlusion times shorter than 3 hrs. Small perfusion deficits of only 20% below required flow caused infarctions at 24 hrs and longer. In the group where the SD-ratio was closer to unity because of a low overall LV-O2-consumption (bradycardia), infarcts at t = 24 hrs were significantly smaller than in the group with a high LV-MVO2.
众所周知，短时间的冠状动脉闭塞不会在犬心脏中产生梗死，但永久性闭塞则总会导致梗死。本文的目的是通过定量直接测量来研究这两种极端情况之间梗死面积的决定因素。我们在闭塞时间介于45分钟至24小时之间时，测量了左心室MV2、冠状动脉和侧支血流以及梗死面积。在一组中，通过使用合成阿片类药物使心率降低来保持低MVO2。在另一组中，通过给予刺激收缩力和心率的合成儿茶酚胺（多巴酚丁胺）来使MV2升高。在所描述的实验条件下，左心室 - 冠状动脉血流反映了对血液和氧气的真实需求。因此，侧支血流与冠状动脉血流的比率（均用示踪微球测量）很好地近似了供需比率（SD）。由于侧支血流在左心室壁上分布不均匀，SD比率也表现出类似的变化。随着冠状动脉闭塞后时间的推移，侧支血流增加，SD比率得到改善。由于高左心室氧需求增加了冠状动脉血流，但对侧支血流几乎没有影响，这种情况对SD比率产生了负面影响。氧需求降低则产生相反的效果。因此，SD比率是受局部和总体氧需求影响的相对和绝对血流不足的有效表达。我们发现SD比率与梗死之间存在显著且具有特征性的相关性，而梗死仅受时间影响。90%的血流不足（即侧支血流 = 所需血流的10%）在闭塞45分钟时会产生50%的梗死（相对于危险区域），但在闭塞3小时及更长时间时会产生90%的梗死。如果灌注不足仅为0.5（侧支血流 = 所需血流的50%），在闭塞时间短于3小时时则检测不到梗死。仅比所需血流低20%的小灌注不足在24小时及更长时间时会导致梗死。在因总体左心室氧消耗低（心动过缓）而使SD比率更接近1的组中，在t = 24小时时的梗死明显小于左心室MVO2高的组。
