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评估二十二碳六烯酸在高血压诱导的犬左心室肥厚模型中的作用。

Evaluation of docosahexaenoic acid in a dog model of hypertension induced left ventricular hypertrophy.

机构信息

Discipline of Physiology, University of Sydney, Anderson Stuart Building (F13), Sydney, NSW, 2006, Australia,

出版信息

J Cardiovasc Transl Res. 2013 Dec;6(6):1000-10. doi: 10.1007/s12265-013-9511-y. Epub 2013 Sep 25.

Abstract

Marine n-3 polyunsaturated fatty acids alter cardiac phospholipids and prevent cardiac pathology in rodents subjected to pressure overload. This approach has not been evaluated in humans or large animals with hypertension-induced pathological hypertrophy. We evaluated docosahexaenoic acid (DHA) in old female dogs with hypertension caused by 16 weeks of aldosterone infusion. Aldosterone-induced hypertension resulted in concentric left ventricular (LV) hypertrophy and impaired diastolic function in placebo-treated dogs. DHA supplementation increased DHA and depleted arachidonic acid in cardiac phospholipids, but did not improve LV parameters compared to placebo. Surprisingly, DHA significantly increased serum aldosterone concentration and blood pressure compared to placebo. Cardiac mitochondrial yield was decreased in placebo-treated hypertensive dogs compared to normal animals, which was prevented by DHA. Extensive analysis of mitochondrial function found no differences between DHA and placebo groups. In conclusion, DHA did not favorably impact mitochondrial or LV function in aldosterone hypertensive dogs.

摘要

海洋 n-3 多不饱和脂肪酸可改变心脏磷脂,预防压力超负荷下啮齿动物的心脏病变。这种方法尚未在高血压诱导病理性肥大的人类或大型动物中进行评估。我们评估了在高血压雌性犬中二十二碳六烯酸(DHA)的作用,这些犬通过 16 周的醛固酮输注导致高血压。醛固酮诱导的高血压导致安慰剂治疗的犬出现向心性左心室(LV)肥大和舒张功能障碍。与安慰剂相比,DHA 补充剂增加了 DHA 并减少了心脏磷脂中的花生四烯酸,但并未改善 LV 参数。令人惊讶的是,与安慰剂相比,DHA 显著增加了血清醛固酮浓度和血压。与正常动物相比,在接受安慰剂治疗的高血压犬中,心脏线粒体产量减少,而 DHA 可预防这种情况。对线粒体功能的广泛分析发现 DHA 组和安慰剂组之间没有差异。总之,DHA 对醛固酮性高血压犬的线粒体或 LV 功能没有有利影响。

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