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目的：研究肾缺血预处理（ＩＰＣ）对心脏电稳定性的影响和机理。方法：２４只大耳白兔随机分为对照组、肾缺血再灌流（Ｉ／Ｒ）组和肾ＩＰＣ＋Ｉ／Ｒ组。观察肾再灌流２４ｈ时及用垂体后叶素（Ｐｔ）和肾上腺素（Ａｄｒ）后的心电图动态变化以及血中一氧化氮（ＮＯ）和心肌中丙二醛（ＭＤＡ）的浓度改变。结果：用Ｐｔ和Ａｄｒ后，肾Ｉ／Ｒ组缺血性ＳＴ段抬高和心律失常发生率同肾ＩＰＣ＋Ｉ／Ｒ组差异显著；肾ＩＰＣ＋Ｉ／Ｒ组ＮＯ代谢物升高和ＭＤＡ降低同Ｉ／Ｒ组差异显著（Ｐ＜０．０５）；除ＭＤＡ外，上述指标在肾ＩＰＣ＋Ｉ／Ｒ组与对照组间差异无显著。结论：肾ＩＰＣ通过减轻心肌缺血性改变使心脏电稳定性增强；ＮＯ可能通过增加氧自由基的清除和扩血管效应而参与此作用。
Objective: To investigate the effect and mechanism of renal ischemic preconditioning (IPC) on cardiac electrical stability. Methods: Twenty - four large white rabbits were randomly divided into control group, renal ischemia - reperfusion (I / R) group and kidney IPC + I / R group. The changes of electrocardiogram (ECG) and nitric oxide (NO) in blood and malondialdehyde (MDA) in myocardium were observed at 24 hours after reperfusion of renal reperfusion and with pituitrin (Pt) and adrenaline (Adr) Results: After treatment with Pt and Adr, the incidence of ischemic ST segment elevation and arrhythmia in renal I / R group were significantly different from those in renal IPC + I / R group. The increase of NO metabolites and the decrease of MDA in renal I / R group were similar to those in I / (P <0.05). There was no significant difference between the IPC + I / R group and the control group except MDA. CONCLUSIONS: Kidney IPC enhances cardiac electrical stability by reducing myocardial ischemic changes; NO may participate in this effect by increasing clearance of oxygen free radicals and vasodilation effects.