食用鱼油可促进大鼠心脏肌力变性。

J M Maixent, A Gerbi, O Barbey, C Lan, I Jamme, H Burnet, A Nouvelot, S Lévy, P J Cozzone, M Bernard
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引用次数: 4

摘要

我们测试了鱼油(FO)饮食促进瓦豆碱正性肌力而不增加毒性的假设。在2个月的时间里,两组成年雄性大鼠分别饲喂1)在饲料中添加鱼油长链多不饱和脂肪酸的常规饲料和2)常规饲料(对照组)。通过(31)P核磁共振波谱法和纯化的膜结合na - k - atp酶,评估两组患者在langendorff灌注心脏中对瓦巴因的反应性。使用沃巴因获得的最大正性肌力几乎是对照组的两倍,并且与能量学的显着变化无关。鱼油组对3 × 10(-4) M沃巴因的功能和能量代谢的改变以及na - k - atp酶的抑制延迟。本研究表明,饲料中的鱼油通过在心膜上掺入n-3多不饱和脂肪酸,促进了乌阿巴因的正性肌力变性,但没有毒性,也没有改变心脏代谢。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dietary fish oil promotes positive inotropy of ouabain in the rat heart.

We tested the hypothesis that a fish oil (FO) diet promotes positive inotropy of ouabain without increased toxicity. For 2 mo, two groups of adult male rats were fed 1) a regular food diet supplemented with dietary long-chain polyunsaturated fatty acid from FO or 2) a regular food diet (control). The responsiveness to ouabain was evaluated for the two groups in Langendorff-perfused hearts, by (31)P nuclear magnetic resonance spectroscopy, and on purified membrane-bound Na-K-ATPase. The maximum positive inotropy achieved with ouabain was nearly two times higher in the FO than in the control group and was not associated with significant changes in energetics. Alteration of function and energetic metabolism and inhibition of Na-K-ATPase in response to 3 x 10(-4) M ouabain were delayed in the FO group. This study demonstrates that dietary FO, by a cardiac membrane incorporation of n-3 polyunsaturated fatty acid, promotes positive inotropy of ouabain without toxicity and changes in cardiac metabolism.

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