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首页> 外文期刊>American Journal of Physiology >Pressure overload-induced LV hypertrophy and dysfunction in mice are exacerbated by congenital NOS3 deficiency.
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Pressure overload-induced LV hypertrophy and dysfunction in mice are exacerbated by congenital NOS3 deficiency.

机译：先天性NOS3缺乏会加剧小鼠压力超负荷引起的LV肥大和功能障碍。

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摘要

To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling induced by chronic pressure overload, the impact of transverse aortic constriction (TAC) on LV structure and function was compared in wild-type (WT) and NOS3-deficient (NOS3(-/-)) mice. Before TAC, LV wall thickness, mass, and fractional shortening were similar in the two mouse strains. Twenty-eight days after TAC, both WT and NOS3(-/-) mice had increased LV wall thickness and mass as well as decreased fractional shortening. Although the pressure gradient across the TAC was similar in both strains of mice 28 days after TAC, LV mass and posterior wall thickness were greater in NOS3(-/-) than in WT mice, whereas fractional shortening and the maximum rate of developed LV pressure were less. Diastolic function, as measured by the time constant of isovolumic relaxation and the maximum rate of LV pressure decay, was impaired to a greater extent in NOS3(-/-) than in WT mice. The degree of myocyte hypertrophy and LV fibrosis was greater in NOS3(-/-) than in WT mice at 28 days after TAC. Mortality was greater in NOS3(-/-) than in WT mice 28 days after TAC. Long-term administration of hydralazine normalized the blood pressure and prevented the LV dilation in NOS3(-/-) mice but did not prevent the LV hypertrophy, dysfunction, and fibrosis associated with NOS3 deficiency after TAC. These results suggest that the absence of NOS3 augments LV dysfunction and remodeling in a murine model of chronic pressure overload.
机译：为了研究内皮一氧化氮合酶（NOS3）在慢性压力超负荷引起的左心室重构中的作用，在野生型（WT）和NOS3中比较了横向主动脉缩窄（TAC）对LV结构和功能的影响-缺陷（NOS3（-/-））小鼠。在TAC之前，两种小鼠品系的LV壁厚，质量和缩短分数相似。 TAC后28天，WT和NOS3（-/-）小鼠的LV壁厚和质量均增加，分数缩短率降低。尽管TAC后28天，两种小鼠的TAC上的压力梯度均相似，但NOS3（-/-）的LV质量和后壁厚度比WT小鼠要大，而分数缩短和最大LV形成率少。通过等容舒张时间常数和最大LV压力衰减率测得的舒张功能在NOS3（-/-）中比在WT小鼠中受到更大程度的损害。 TAC后28天，NOS3（-/-）中的心肌细胞肥大和LV纤维化程度大于WT小鼠。 TAC后28天，NOS3（-/-）中的死亡率高于野生型小鼠。长期服用肼苯哒嗪可使血压正常化，并阻止了NOS3（-/-）小鼠的左室扩张，但并未阻止左室肥大后左室肥大，功能障碍和与NOS3缺乏相关的纤维化。这些结果表明，在慢性压力超负荷的小鼠模型中，NOS3的缺乏会加剧LV功能障碍和重塑。

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