...
首页> 外文期刊>Revista Brasileira de Medicina do Esporte >Efeito da administra??o oral de arginina sobre a press?o arterial e parametros cardíacos em ratos submetidos ao bloqueio cr?nico da síntese de óxido nítrico
【24h】

Efeito da administra??o oral de arginina sobre a press?o arterial e parametros cardíacos em ratos submetidos ao bloqueio cr?nico da síntese de óxido nítrico

机译:精氨酸对慢性阻滞一氧化氮合成的大鼠血压和心脏参数的影响

获取原文
   

获取外文期刊封面封底 >>

       

摘要

It has been clearly established that chronic inhibition of nitric oxide synthesis results in a sustained increase in blood pressure, cardiac remodeling and fibrosis. It was also demonstrated by our group that arginine supplementation was able to increase the skeletal muscle resistance to fatigue, but its mechanism remains uncertain. The experimental treatment of rats with L-NAME is one of the most common models employed to induce hypertension. The expected compensatory response against increases in systemic vascular resistance would be ventricular hypertrophy. However, the presence of cardiac hypertrophy still controversial. The aim of the present study was to verify the effects of nitric oxide inhibition through oral L-NAME administration on the cardiac tissue of rats, and the possible reversion by L-arginine. Thirty male Wistar rats (250-350 g) were kept in controlled conditions of temperature, light, humidity, with water and food "ad libitum". At the end of 4 weeks or treatments the animals were sacrificed by CO2 inhalation and the hearts were removed. Soon after, the hearts were dissected, to separate atria and ventricules, obtaining the total heart weight. After the retreat of the right ventricule, the remaining part was weighed, to obtain the left ventricular weight (LVW, mg); the difference between the total heart weight and the LVW was considered the right ventricular weight (RVW, mg). These values were corrected in function of the corporal weight obtained in the last week of treatment. L-NAME was able to induced hypertension and increases in double product but without any heart hypertrophy. The increase arterial pressure and double product were reversed by L-arginine administration in a dose-dependent way. Preliminary findings demonstrated a reversion of heart fibroses induced by L-NAME, after arginine treatment. We concluded that arginine may constitute a valuable tool in preventing hypertension and cardiac remodeling mainly related to vascular dysfunctions and maybe also in athletic activities.
机译:已经清楚地确定,一氧化氮合成的慢性抑制导致血压,心脏重塑和纤维化的持续增加。我们的研究小组还证明,补充精氨酸能够增加骨骼肌对疲劳的抵抗力,但其机制仍不确定。用L-NAME对大鼠进行实验性治疗是诱发高血压的最常见模型之一。针对全身血管阻力增加的预期补偿反应将是心室肥大。但是,心脏肥大的存在仍存在争议。本研究的目的是验证通过口服L-NAME给药对大鼠心脏组织产生的一氧化氮抑制作用,以及L-精氨酸可能逆转的作用。将30只雄性Wistar大鼠(250-350g)保持在温度,光照,湿度,水和食物“随意”的受控条件下。在4周或治疗结束时,通过吸入CO 2处死动物并移出心脏。不久之后,解剖心脏,将心房和心室分开,获得心脏的总重量。右室退缩后,称重其余部分,得到左心室重量(LVW,mg)。总心脏重量和左室重量之间的差异被认为是右心室重量(RVW,毫克)。根据在治疗的最后一周获得的体重来校正这些值。 L-NAME能够诱发高血压并增加了两倍的乘积,但没有任何心脏肥大。通过L-精氨酸给药以剂量依赖的方式逆转了动脉压的升高和双重产物。初步发现表明,精氨酸治疗后,L-NAME诱导的心脏纤维逆转。我们得出的结论是,精氨酸可能是预防高血压和心脏重塑的重要工具,而高血压和心脏重塑主要与血管功能障碍有关,也可能与体育活动有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号