Walker D M, Walker J M, Yellon D M
Hatter Institute for Cardiovascular Studies, Division of Cardiology, University College Hospital, London.
Cardioscience. 1993 Dec;4(4):263-6.
Many investigators use in vitro models of global ischemia to examine the effects of preconditioning, often with recovery of contractile function as the end-point. Such models are relevant to myocardial protection during cardiac surgery. However, there is still debate as to whether preconditioning preserves ventricular contraction secondary to limitation of infarction or by a direct effect on stunning. Since infarct size is the original end-point against which protection by preconditioning is measured, our aims were, first, to validate global ischemic preconditioning by measuring infarct size after subsequent regional ischemia and, second, to correlate limitation of infarct size with mechanical function. After stabilization, seven isolated buffer perfused rabbit hearts were subjected to 5 minutes of global "no-flow" ischemia followed by 10 minutes of reperfusion ("global preconditioning"). Seven control hearts were allowed to stabilize for an additional 15 minutes at constant flow. Subsequently, regional ischemia was induced in both groups for 45 minutes followed by 2 hours of reperfusion. Left ventricular and coronary perfusion pressures were measured throughout. Myocardial infarct size was measured using triphenyltetrazolium staining and expressed as a percentage of the area at risk outlined with fluorescent microspheres. The ratio of infarct to risk zone was reduced from 47.6 +/- 7.3% in control hearts to 16.4 +/- 5.4% (p = 0.005) in preconditioned hearts, confirming the efficacy of global preconditioning. In addition, preconditioning led to a better preservation of systolic function, which correlated significantly with limitation of infarct size (r = 0.75, p = 0.002). Global preconditioning may account for the successful use of cross-clamp fibrillation during cardiac surgery.
许多研究人员使用全脑缺血的体外模型来研究预处理的效果,通常以收缩功能的恢复作为终点。此类模型与心脏手术期间的心肌保护相关。然而,关于预处理是通过限制梗死面积还是通过对心肌顿抑的直接作用来保留心室收缩功能,仍存在争议。由于梗死面积是衡量预处理保护作用的原始终点,我们的目的,首先是通过测量后续局部缺血后的梗死面积来验证全脑缺血预处理,其次是将梗死面积的限制与机械功能相关联。稳定后,七只离体缓冲液灌注兔心先经历5分钟的全脑“无血流”缺血,随后再灌注10分钟(“全脑预处理”)。七只对照心脏在恒定血流下再稳定15分钟。随后,两组均诱导局部缺血45分钟,然后再灌注2小时。全程测量左心室和冠状动脉灌注压力。使用三苯基四氮唑染色测量心肌梗死面积,并表示为荧光微球勾勒出的危险区域面积的百分比。梗死与危险区域的比例从对照心脏的47.6±7.3%降至预处理心脏的16.4±5.4%(p = 0.005),证实了全脑预处理的有效性。此外,预处理导致收缩功能得到更好的保留,这与梗死面积的限制显著相关(r = 0.75,p = 0.002)。全脑预处理可能解释了心脏手术期间交叉夹闭房颤的成功应用。