氙气预处理对未成熟心肌缺血/再灌注损伤及氧化应激的影响

目的 观察氙气预处理对未成熟心肌缺血再灌注（I/R）损伤的保护作用，并对其作用机制进行探讨。方法 采用离体心脏灌流模型，将48只离体灌注的幼兔心脏随机分为4组（每组12只）:对照组（予以持续灌注300 min）、I/R组（灌注60 min后，缺血60 min，复灌180 min）、氙气预处理组〔分为2个亚组，分别用1倍肺泡最小有效浓度（MAC）、0.5 MAC氙气预处理心脏后，缺血60 min，复灌180 min〕。检测复灌后各组心脏功能、心肌梗死面积、线粒体结构、超氧化物歧化酶（SOD）和丙二醛（MDA）水平。结果 与I/R组相比，1 MAC和0.5 MAC氙气预处理均提高心脏功能（P<0.01），减少心肌梗死面积（P<0.01），降低线粒体评分（P<0.01），增加心肌SOD活性（P<0.05）并降低MDA含量（P<0.05）。1 MAC和0.5 MAC氙气预处理组各项指标比较差异均无统计学意义（P>0.05）。结论 1 MAC和0.5 MAC氙气预处理均能减少离体灌注的未成熟心肌I/R损伤。减轻氧化应激是氙气发挥保护作用的可能机制之一。

Effects of Xenon Preconditioning Against Ischemia/Reperfusion Injury and Oxidative Stress in Immature Heart

Objective To investigate whether xenon preconditioning (PC) could protect immature myocardium against ischemia-reperfusion (I/R) injury in a dose-dependent manner and clarify the role of xenon PC on oxidative stress. Methods Forty-eight isolated perfused immature rabbit hearts were randomly divided into four groups (n=12): The sham group had the hearts perfused continuously for 300 min. In I/R group, the hearts were subjected to 60 min perfusion followed by 60 min ischemia and 180 min reperfusion. In 1 minimum alveolar concentration (MAC) and 0.5 MAC xenon PC groups, the hearts were preconditioned with 1 MAC or 0.5 MAC xenon respectively, following 60 min ischemia and 180 min reperfusion. The cardiac function, myocardial infarct size, mitochondrial structure, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level in each group were determined after reperfusion. Results Compared with I/R group, both 1 MAC and 0.5 MAC xenon preconditioning significantly improved cardiac function (P<0.01), reduced myocardial infarct size (P<0.01) and mitochondrial damage, increased SOD activity and decreased MDA level (P<0.01). There were no differences between 1 MAC group and 0.5 MAC xenon group (P>0.05). Conclusion Xenon preconditioning at 0.5 and 1 MAC produce similar cardioprotective effects against I/R injury in isolated perfused immature heart.