Hoffmeister H M, Ströbele M, Bässler A, Beyer M E, Kazmaier S, Seipel L
Medizinische Universitätsklinik, Abt. III, Tübingen, Germany.
Basic Res Cardiol. 1998 Dec;93(6):487-96. doi: 10.1007/s003950050119.
A reduction in coronary flow leads to a parallel decrease in contractile function. Thus, a flow/function balance is established in the myocardium under certain circumstances avoiding the development of a necrosis (referred to as "hibernating" myocardium). The impact of a preconditioning period on this critical balance was examined.
In 116 isovolumetrically beating rat hearts, 3 h of hypoperfusion with 15% of control coronary flow were performed followed by 1 h reperfusion; 40 hearts served as controls. As a preconditioning period, in half of the rat hearts a 5 min no-flow ischemia followed by 10 min reperfusion was performed, preceding the prolonged hypoperfusion.
Systolic function was identically reduced in both groups after 3 h hypoperfusion (LVP: 39 +/- 2 mmHg, 40 +/- 2 mmHg vs. controls 90 +/- 3 mmHg; p < 0.01). Without preconditioning hypoperfusion resulted in a marked initial decrease in function. This period was followed by an adaptation to a higher steady state level of function compared with non-preconditioned hypoperfused hearts (p < 0.05). After preconditioning hypoperfusion directly resulted in this level of contraction. Contractile reserve was reduced (p < 0.01) identically in both hypoperfusion groups. Adenine nucleotides were decreased (p < 0.01) after 3 h hypoperfusion to 2.1 +/- 0.2 mumol/gww vs. controls (4.7 +/- 0.2 mumol/gww). After initial preconditioning adenine nucleotides were better preserved (3.2 +/- 0.2 mumol/gww) going ahead with a creatine phosphate overshoot of 126% (p < 0.01). After reperfusion, systolic function and contractile reserve were identical in both groups.
A period of preceding no-flow ischemia followed by reperfusion modifies functional adaptation to hypoperfusion and preserves high energy phosphates. Therefore, the metabolic balance during hypoperfusion is improved by preconditioning, although no impact on contractile reserve or the functional status of reperfused myocardium after low-flow ischemia can be seen.
冠状动脉血流减少会导致收缩功能平行下降。因此，在某些情况下，心肌中会建立血流/功能平衡，避免坏死（称为“冬眠”心肌）的发生。研究了预处理期对这种关键平衡的影响。
在116只等容跳动的大鼠心脏中，用对照冠状动脉血流的15%进行3小时的低灌注，随后进行1小时再灌注；40只心脏作为对照。作为预处理期，在一半的大鼠心脏中，在长时间低灌注之前，先进行5分钟无血流缺血，然后进行10分钟再灌注。
3小时低灌注后，两组的收缩功能均同等降低（左心室压：39±2 mmHg，40±2 mmHg，对照组为90±3 mmHg；p<0.01）。未进行预处理时，低灌注导致功能明显初始下降。与未预处理的低灌注心脏相比，此阶段之后会适应更高的稳定功能水平（p<0.05）。预处理后，低灌注直接导致此收缩水平。两个低灌注组的收缩储备均同等降低（p<0.01）。3小时低灌注后，腺嘌呤核苷酸降低（p<0.01）至2.1±0.2 μmol/g湿重，而对照组为（4.7±0.2 μmol/g湿重）。初始预处理后，腺嘌呤核苷酸得到更好的保存（3.2±0.2 μmol/g湿重），同时磷酸肌酸超射126%（p<0.01）。再灌注后，两组的收缩功能和收缩储备相同。
先进行一段时间的无血流缺血再灌注可改变对低灌注的功能适应并保存高能磷酸盐。因此，预处理可改善低灌注期间的代谢平衡，尽管未见对收缩储备或低流量缺血后再灌注心肌的功能状态有影响。
