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本实验用高效液相色谱法测定了不同缺血／再灌注条件下心肌组织内高能磷酸化合物的含量，并用放色法测定了大鼠心肌组织内血管紧张素Ⅱ（ＡＴ－Ⅱ）的含量。结果表明：缺血３０ｍｉｎ和缺血４０ｍｉｎ组ＡＴ－Ⅱ明显高于缺血１５ｍｉｎ组（Ｐ＜０．０５），再灌后ＡＴ－Ⅱ含量进一步升高，此变化与在缺血再灌注过程中的高能磷酸化合物改变恰好相反。在缺血４０ｍｉｎ再灌２０ｍｉｎ组的灌流液中预先加入血管紧张素转换酶抑制剂－巯甲丙脯酸，则心肌中磷酸肌酸（ＰＣｒ）、三磷酸腺苷（ＡＴＰ），ＴＡＮ（ＡＭＰ＋ＡＤＰ＋ＡＴＰ）与能荷Ｅ（１／２ＡＤＰ＋ＡＴＰ／ＴＡＮ）均非常显著高于未加巯甲丙脯酸组（Ｐ＜０．００１），可见心肌缺血／再灌注时心肌高能磷酸化合物含量的变化与肾素－血管紧张素系统关系密切，两者呈显著负相关（ｒ＝－０．８３）。抑制ＡＴ－Ⅱ的生成能有效地保护缺血心肌的能量贮备
In this study, high-performance liquid chromatography was used to determine the content of high-energy phosphate compounds in myocardial tissue under different ischemia / reperfusion conditions. The content of AT-Ⅱ in myocardium of rats was determined by colorimetry. The results showed that AT-Ⅱ in 30min and 40min ischemia group was significantly higher than that in ischemia 15min group (P <0.05), and the content of AT-Ⅱ increased further after reperfusion. The change in high-energy phosphate compounds is just the opposite. ATP, TAN (AMP + ADP + ATP) and energy load in cardiac muscle were pre-treated with angiotensin converting enzyme inhibitor-captopril in the perfusion fluid of 40min ischemia and 40min reperfusion. E (1 / 2ADP + ATP / TAN) were significantly higher than those in the group without captopril (P <0.001). The change of myocardial high-energy phosphoric acid Vegetarian system is closely related, the two showed a significant negative correlation (r = -0.83). Inhibition of AT-Ⅱ production can effectively protect the ischemic myocardium energy reserve