Müller K D, Sass S, Gottwik M G, Schaper W
Basic Res Cardiol. 1982 Mar-Apr;77(2):170-81. doi: 10.1007/BF01908170.
The influence of myocardial oxygen consumption (MVO2) at the moment of coronary occlusion on the size of the ensuing necrosis was investigated in 12 anaesthetised dogs. A two-infarction model was used with a sequential occlusion of two distant coronary branches in the same heart, however under different levels of MVO2. One group of occlusions was produced at a high MVO2 of 21.6 +/- 3.0 ml O2 . min-1 . 100 g-1. This group was compared with a second in which necrosis proceeded at a low MVO2 estimated to be 5.9 +/- 1.5 ml O2 . min-1 . 100 g-1 averaged over a 90-min occlusion period. Infarct size expressed as percentage of perfusion area was 43 +/- 28% in group 1 and 11 +/- 11% in group 2 (p less than 0.005). The mass of the perfusion area was equal in both groups (17 +/- 4 g, 19 +/- 6 g). The amount of myocardial necrosis, which after a 90-min occlusion depends on the acute collateral blood flow, was in every case greater under high MVO2. Thus a low MVO2 at the moment of occlusion can postpone myocardial necrosis.
在12只麻醉犬中研究了冠状动脉闭塞瞬间心肌耗氧量（MVO2）对随后坏死面积大小的影响。采用双梗死模型，在同一心脏中依次闭塞两个 distant 冠状动脉分支，但处于不同的MVO2水平。一组闭塞在高MVO2（21.6±3.0 ml O2·min-1·100 g-1）下产生。将该组与另一组进行比较，在第二组中，坏死在低MVO2下进行，估计在90分钟闭塞期内平均为5.9±1.5 ml O2·min-1·100 g-1。以灌注面积百分比表示的梗死面积在第1组中为43±28%，在第2组中为11±11%（p＜0.005）。两组的灌注面积质量相等（17±4 g，19±6 g）。在90分钟闭塞后，心肌坏死量取决于急性侧支血流量，在高MVO2下，每种情况下坏死量都更大。因此，闭塞瞬间的低MVO2可延缓心肌坏死。
