To investigate the effect of hydrogen-rich water on myocardial tissue metabolism in a myocardial ischemia-reperfusion injury (MIRI) rat model. Twelve rats were randomly divided into a hydrogen-rich water group and a control group of size 6 each. After the heart was removed, it was fixed in the Langendorff device, and the heart was perfused with 37 °C perfusion solution pre-balanced with oxygen. The control group was perfused with Kreb’s-Ringers (K-R) solution, and the hydrogen-rich water group was perfused with K-R solution + hydrogen-rich water. Liquid Chromatograph Mass Spectrometer (LC-MS) analysis platform was used for metabolomics research. Principle component analysis (PCA), partial least squares discriminant analysis (PLS-DA), orthogonal partial least squares discriminant analysis (OPLS-DA), Variable importance in projection (VIP) value of OPLS-DA model (threshold value ≥1) were employed with independent sample T Test (p < 0.05) to find differentially expressed metabolites, and screen for differential metabolic pathways. VIP (OPLS-DA) analysis was performed with T test, and the metabolites of the control group and the hydrogen-rich water group were significantly different, and the glycerophospholipid metabolism was screened. Seven myocardial ischemia-reperfusion injury (MIRI)-related signaling pathways were identified, including glycerophospholipid metabolism, glycosylphosphatidylinositol (GPI) anchored biosynthesis, and purine metabolism, as well as 10 biomarkers such as phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine. Hydrogen-rich water regulates the metabolic imbalance that could change MIRI myocardial tissue metabolism, and alleviate ischemia-reperfusion injury in isolated hearts of rats through multiple signaling pathways.

在心肌缺血再灌注损伤（MIRI）大鼠模型中调查富氢水对心肌组织代谢的影响。将十二只大鼠随机分为每只大小为6的富氢水组和对照组。取出心脏后，将其固定在Langendorff装置中，然后用预先平衡有氧的37°C灌注溶液灌注心脏。对照组灌注Kreb's-Ringers（KR）溶液，富氢水组灌注KR溶液+富氢水。液相色谱质谱仪（LC-MS）分析平台用于代谢组学研究。主成分分析（PCA），偏最小二乘判别分析（PLS-DA），正交偏最小二乘判别分析（OPLS-DA），p <0.05）查找差异表达的代谢产物，并筛选差异代谢途径。采用T检验进行VIP（OPLS-DA）分析，对照组和富氢水组的代谢产物明显不同，并筛选了甘油磷脂代谢。确定了七个与心肌缺血再灌注损伤（MIRI）相关的信号传导途径，包括甘油磷脂代谢，糖基磷脂酰肌醇（GPI）锚定的生物合成和嘌呤代谢，以及10个生物标记物，如磷脂酰胆碱，磷脂酰乙醇胺和磷脂酰丝氨酸。富氢水调节可能改变MIRI心肌组织代谢的代谢失衡，并通过多种信号途径减轻离体大鼠心脏的缺血再灌注损伤。