结论：缺血后处理可减轻缺血再灌注损伤、其机制可能与减少心肌细胞凋亡有关。

CONCLUSION: ischemic postconditioning can relieve the ischemic reperfusion injury, the mechanism of which may be related with the decreased myocardial apoptosis.

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因此，我们通过鼠来研究是否吸入氢气减轻缺血再灌注损伤来起到心脏保护作用。

Therefore, we investigate whether H2 gas confers cardioprotection against ischemia–reperfusion injury in rats.

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因此，在冠脉血运重建时，氢气吸入将成为一种减轻缺血再灌注损伤的非常有希望的措施。

Inhalation of H2 gas at incombustible levels during ischemia and reperfusion reduces infarct size without altering hemodynamic parameters, thereby preventing deleterious left ventricular remodeling.

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