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为探讨缺血预处理延迟保护作用的非缺血诱导方式，我们在离体大鼠心脏等容收缩灌流模型上观察到：24小时前腹腔注射ZnS4诱导心肌金属硫蛋白（MT）含量增高1．6倍；与单纯缺血再灌注组比较，诱导MT组显著减少了肌红蛋白漏出和MDA增加，减轻了心肌ATP耗竭，增强了左室做功能力，但不影响冠脉流量。因此我们认为，ZnSO4注射诱导MT合成，能代替缺血预处理，模拟出缺血预处理的延迟保护作用。
To investigate the non-ischemic induction of delayed protection of ischemic preconditioning, we observed that the intramembranous injection of ZnS4 induced an increase in myocardial metallothionein (MT) levels 24 hours prior to isovolumic contractile perfusion in isolated rat hearts. Compared with the ischemia-reperfusion group, the induction of MT significantly reduced the leakage of myoglobin and the increase of MDA, reduced the myocardial ATP depletion and enhanced the function of the left ventricle, but did not affect the coronary flow. Therefore, we believe that ZnSO4 injection induces MT synthesis, which can replace the ischemic preconditioning and simulate the delayed protection of ischemic preconditioning.