摘要
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）。
The changes of high energy phosphates and AT-Ⅱ content were measured by HPLC and radioimmunoassy in different time phases during ischemia and reperfusion in isolated heart of Langendorff perfused rat.The results indicated that the AT-Ⅱ content of myocardium in ischemia 30 and 40min group were much higher than that of ischemia 15min group(P<0.05).But it was even much higher in reperfusion group folloming ischemia 30min,40min,than the corresponding ischemia groups.The change of AT-Ⅱconcentration appeared contrary to the change of adenine nucleotides level,ACEI-captopril group(ischemia 40min/reperfusion 20min+captopril) has much higher PCr,ATP,TAN and E than untreated group.Taken these two paramenters together,it’s quite apparant that the adenine nucleotides contents inmyocardium during ischemia/reperfusion showed negative correlation(r=-0.83)to AT-Ⅱcontent.Inhibit production of AT-Ⅱwould protect the energy reserve and prevent the developing of reperfusion injury.
出处
《中国病理生理杂志》
CSCD
北大核心
1996年第3期263-266,共4页
Chinese Journal of Pathophysiology
关键词
心肌缺血
能量代谢
血管紧张素
再灌注
Myocardium.Energy metabolism.Angiotensins.Captopril.Rats
