Kawashima S, Satani A, Tsumoto S, Kondo T, Ikeoka K, Morita M, Iwasaki T
First Department of Medicine, Hyogo College of Medicine, Japan.
Cardiovasc Res. 1991 Oct;25(10):837-43. doi: 10.1093/cvr/25.10.837.
The aim was to study coronary pressure-flow, pressure-myocardial wall motion and myocardial wall motion-myocardial oxygen consumption relations in postischaemic myocardium with prolonged myocardial dysfunction (stunned myocardium) in comparison with normal myocardium.
Regional myocardial wall thickening was measured with ultrasonic crystals, and postischaemic myocardial dysfunction was achieved by occlusion of a carotid-left anterior descending coronary artery bypass (15 min) and reperfusion (30 min). Coronary perfusion pressure was decreased in 10 mm Hg steps by constricting the bypass before and after producing postischaemic myocardial dysfunction. At each constriction step, coronary flow, regional wall thickening, and regional myocardial oxygen consumption in the area perfused by the left anterior descending artery were measured.
12 anaesthetised open chest mongrel dogs, weighing 12-16 kg, were studied.
At the basal level, myocardial wall thickening of postischaemic myocardium was depressed compared to normal myocardium, at 18.5(SD 8.9)% v 1.3(7.1)%, p less than 0.01. With coronary stenosis, wall thickening gradually decreased at a coronary pressure below 60 mm Hg in normal myocardium, but remained unchanged until mean coronary pressure was reduced to 50 mm Hg in postischaemic myocardium. Myocardial wall thickening of postischaemic myocardium was always more depressed than normal myocardium. At any level of coronary pressure, coronary flow in postischaemic myocardium was not different from normal myocardium. There was no difference in regional myocardial oxygen consumption between normal and postischaemic myocardium at any level of coronary pressure. However, regional myocardial oxygen consumption in postischaemic myocardium was higher than in normal myocardium performing similar levels of myocardial wall thickening.
The coronary pressure-function relation but not the pressure-flow relation changed in postischaemic myocardium after a 15 min coronary occlusion. Regional myocardial oxygen consumption was relatively increased in postischaemic myocardium.
旨在研究与正常心肌相比,长时间心肌功能障碍(心肌顿抑)的缺血后心肌中的冠状动脉压力-血流、压力-心肌壁运动和心肌壁运动-心肌氧耗关系。
用超声晶体测量局部心肌壁增厚情况,通过阻断颈动脉-左前降支冠状动脉搭桥(15分钟)并再灌注(30分钟)造成缺血后心肌功能障碍。在产生缺血后心肌功能障碍前后,通过收缩搭桥血管使冠状动脉灌注压力以10mmHg的步长降低。在每个收缩步骤,测量左前降支灌注区域的冠状动脉血流、局部壁增厚和局部心肌氧耗。
研究了12只体重12-16kg的麻醉开胸杂种狗。
在基础水平,缺血后心肌的心肌壁增厚低于正常心肌,分别为18.5(标准差8.9)%对1.3(7.1)%,p<0.01。随着冠状动脉狭窄,正常心肌在冠状动脉压力低于60mmHg时壁增厚逐渐降低,但缺血后心肌在平均冠状动脉压力降至50mmHg之前保持不变。缺血后心肌的心肌壁增厚始终比正常心肌更受抑制。在任何冠状动脉压力水平,缺血后心肌的冠状动脉血流与正常心肌无差异。在任何冠状动脉压力水平,正常心肌和缺血后心肌的局部心肌氧耗无差异。然而,在进行相似程度心肌壁增厚时,缺血后心肌的局部心肌氧耗高于正常心肌。
冠状动脉闭塞15分钟后,缺血后心肌的冠状动脉压力-功能关系而非压力-血流关系发生改变。缺血后心肌的局部心肌氧耗相对增加。