Zile M R, Neill W A, Gaasch W H, Oxendine J, Apstein C S, Weinberg E, Bing O H
Department of Medicine (Cardiology), Tufts University School of Medicine, Boston, MA.
J Mol Cell Cardiol. 1987 Oct;19(10):977-89. doi: 10.1016/s0022-2828(87)80570-9.
During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37 degrees C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37 degrees C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (n = 9) or 90 mins (n = 9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67 +/- 1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33 +/- 0.18, the LV end diastolic pressure was 7.5 +/- 0.4 mmHg, and mean transmural myocardial adenosine triphosphate (ATP) was 16.4 +/- 1.1 microM/g DW. At the onset and throughout the first 45 mins of ischemia (n = 9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26 +/- 1.6 micron/g DW). After 75 mins of ischemia (n = 9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76 +/- 0.5 microM/g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82 +/- 2.0% and the subendocardial to subepicardial flow ratio was 1.75 +/- 0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure greater than 60 mmHg, n = 4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.
在长时间缺血性心脏骤停期间，成功的心肌保护取决于心脏停搏液均匀地输送到心脏的所有区域。因此，我们研究了在18个离体血液灌注犬心脏（等容左心室）的常温（37℃）缺血期间，一种中性晶体液（右旋糖酐 - 盐水）的区域和透壁分布情况。在基础状态下，冠状动脉灌注压为100mmHg。在缺血开始时以及整个缺血过程中每隔15分钟，我们以100mmHg的灌注压输注100ml晶体液（37℃），并评估晶体液的分布情况（放射性微球技术）。缺血60分钟（n = 9）或90分钟（n = 9）后对心脏进行再灌注。在基础的心脏骤停前状态，左心室（LV）接受总冠状动脉血流量的67±1.0%；LV心内膜下与心外膜下血流比值为1.33±0.18，LV舒张末期压力为7.5±0.4mmHg，平均透壁心肌三磷酸腺苷（ATP）为16.4±1.1μmol/g干重。在缺血开始时以及缺血的前45分钟内（n = 9），晶体液的区域和透壁分布与基础状态下冠状动脉血流的分布相似；LV舒张末期压力没有变化，但ATP含量有适度下降（7.26±1.6μmol/g干重）。缺血75分钟后（n = 9），尽管出现了缺血性挛缩（所有9个心脏的LV舒张末期压力均超过20mmHg）且ATP显著耗竭（2.76±0.5μmol/g干重），但整个LV尤其是心内膜下的晶体液输送量增加（LV接受82±2.0%，心内膜下与心外膜下血流比值为1.75±0.1）。即使在缺血性心脏骤停期间存在严重挛缩的亚组中（LV舒张末期压力大于60mmHg，n = 4），晶体液的输送也没有减少。因此，缺血性挛缩的存在并不妨碍晶体液输送到LV心内膜下。
