Gupta M, Gameiro A, Singal P K
Can J Physiol Pharmacol. 1987 Jun;65(6):1157-64. doi: 10.1139/y87-183.
Effects of xanthine--xanthine oxidase produced oxygen radicals were studied in hypertrophied rat hearts in a Langendorff preparation. Heart hypertrophy was produced by banding of the abdominal aorta for 6 weeks. This resulted in a 22% increase in ventricle/body weight ratio compared with that of sham-operated controls. Perfusion with xanthine--xanthine oxidase caused contractile failure and a significant rise in the resting tension. Complete contractile failure in hypertrophied hearts was seen at 25.5 +/- 3.2 min, whereas in control hearts it happened at 14.4 +/- 5.6 min. Contractile failure due to oxygen radicals in both groups was associated with a decline in high energy phosphates, increased lipid peroxidation, and extensive structural damage. Sarcolemma in both groups became permeable to the extracellular tracer lanthanum. As compared with control, in hypertrophied hearts the malondialdehyde content, indicative of lipid peroxidation, was less by 40%; whereas superoxide dismutase, a free radical scavenger, was higher by a similar amount. These data show a greater capacity of the 6-week hypertrophied heart to withstand a free radical induced contractile failure. This delay in oxygen radical effect can be partially explained by the reduced lipid peroxide content and increased superoxide dismutase activity in the hypertrophied hearts.
在Langendorff离体心脏灌流装置中，研究了黄嘌呤 - 黄嘌呤氧化酶产生的氧自由基对大鼠肥厚心脏的影响。通过结扎腹主动脉6周诱导心脏肥大。与假手术对照组相比，这导致心室/体重比增加了22%。用黄嘌呤 - 黄嘌呤氧化酶灌流会导致收缩功能衰竭以及静息张力显著升高。肥厚心脏在25.5±3.2分钟时出现完全收缩功能衰竭，而对照心脏在14.4±5.6分钟时出现。两组中由氧自由基导致的收缩功能衰竭均与高能磷酸盐减少、脂质过氧化增加以及广泛的结构损伤有关。两组的肌膜对细胞外示踪剂镧均具有通透性。与对照组相比，肥厚心脏中指示脂质过氧化的丙二醛含量降低了40%；而自由基清除剂超氧化物歧化酶的含量则升高了类似的幅度。这些数据表明，6周龄的肥厚心脏具有更强的能力来抵抗自由基诱导的收缩功能衰竭。肥厚心脏中脂质过氧化物含量降低以及超氧化物歧化酶活性增加，这可以部分解释氧自由基作用的延迟。
