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一氧化氮合成阻断会增加进行有氧训练的大鼠的心肌肥大和心脏纤维化。

Nitric oxide synthesis blockade increases hypertrophy and cardiac fibrosis in rats submitted to aerobic training.

作者信息

Souza Hugo Celso Dutra de, Penteado Daniel Martins Dias, Martin-Pinge Marli Cardoso, Barbosa Neto Octávio, Teixeira Vicente de Paula Antunes, Blanco João Henrique Dutra, Silva Valdo José Dias da

机构信息

Faculdade de Medicina de Ribeirão Preto, Universidade Estadual de Londrina, Uberaba, MG, Brazil.

出版信息

Arq Bras Cardiol. 2007 Aug;89(2):88-93, 99-104. doi: 10.1590/s0066-782x2007001400005.

Abstract

OBJECTIVE

The objective of the present study was to evaluate cardiac tissue adaptations in rats submitted to aerobic training after nitric oxide (NO) synthesis blockade.

METHODS

The animals (n=48) were divided into four groups: sedentary (CONTROL group); hypertensive after administration of NG-nitro-L-arginine methyl ester for 7 days (L-NAME Group); trained for 8 weeks through swimming exercises (TRAINED Group);trained and treated with L-NAME during the last week (L-NAME TRAINED Group). All the animals were submitted to the experiment procedures for blood pressure (BP) readings and cardiac morphometric evaluation.

RESULTS

In comparison to the other groups, the L-NAME and L-NAME TRAINED groups were hypertensive (p<0.05); however, BP elevation in the L-NAME TRAINED group was significantly lower than the L-NAME group (p<0.05). The heart weight indexes for the TRAINED and L-NAME TRAINED groups were higher than the CONTROL and L-NAME groups (p<0.05). Also they had presented higher rates of macroscopic cardiac area and cardiac fibrosis in relation to the rest (p<0.05); comparisons revealed that the values for the L-NAME TRAINED group were significantly higher (p<0.05) than the others.

CONCLUSION

Short term NO synthesis blockade in sedentary animals induced hypertension but did not cause cardiac hypertrophy. In the trained animals, the inhibition of NO synthesis attenuated hypertension, induced cardiac hypertrophy and significantly increased myocardial fibrosis, indicating that NO plays an important role in cardiac tissue adaptations caused by aerobic exercise.

摘要

目的

本研究的目的是评估一氧化氮(NO)合成被阻断后进行有氧训练的大鼠心脏组织的适应性变化。

方法

将动物(n = 48)分为四组:久坐不动组(对照组);给予NG-硝基-L-精氨酸甲酯7天后的高血压组(L-NAME组);通过游泳训练8周的训练组(训练组);在最后一周接受L-NAME训练和治疗的组(L-NAME训练组)。所有动物均接受实验程序以测量血压(BP)并进行心脏形态学评估。

结果

与其他组相比,L-NAME组和L-NAME训练组血压升高(p<0.05);然而,L-NAME训练组的血压升高明显低于L-NAME组(p<0.05)。训练组和L-NAME训练组的心脏重量指数高于对照组和L-NAME组(p<0.05)。此外,与其他组相比,它们的宏观心脏面积和心脏纤维化率更高(p<0.05);比较显示,L-NAME训练组的值明显高于其他组(p<0.05)。

结论

久坐不动的动物短期NO合成被阻断会导致高血压,但不会引起心脏肥大。在经过训练的动物中,NO合成的抑制减轻了高血压,诱导了心脏肥大并显著增加了心肌纤维化,表明NO在有氧运动引起的心脏组织适应性变化中起重要作用。

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