摘要
背景:雷诺嗪通常用于治疗有症状的慢性稳定型心绞痛患者的心绞痛症状。通过改善缺血再灌注,还观察到雷诺嗪对动物模型中的心肌缺血性损伤具有保护作用。值得注意的是找到可以减少该药物的副作用并因此增加其临床应用的干预措施。 方法:在本报告中,我们使用慢性缺血性心力衰竭(CHF)大鼠模型来检查迷走神经刺激是否可以增强雷诺嗪对CHF心脏功能恶化的影响。血浆去甲肾上腺素(NE)和脑利钠肽[BNP,在大鼠中称为B型利尿钠肽-45(BNP-45)]受交感神经活动调节。因为NE和BNP被认为是指示心力衰竭进展的神经激素,我们还确定了除心脏功能之外的血浆NE和BNP-45的水平。此外,我们检查了交感神经促炎细胞因子在迷走神经激活参与中的作用。 结果:我们的数据显示雷诺嗪腹腔注射改善了左心室功能受损,并减弱了CHF发生后过度的NE / BNP-45和细胞因子(如IL-1β,IL-6和TNF-α)。特别是,我们的结果表明迷走神经激活很大程度上放大了雷诺嗪对CHF心脏功能的影响。 结论:我们的数据表明:1)雷诺嗪缓解交感神经活动,从而改善CHF心脏功能恶化; 2)迷走神经刺激增强雷诺嗪的作用。因此,该研究的结果对于迷走神经刺激和雷诺嗪组合在改善CHF心脏功能中所起的作用具有意义。
关键词: 迷走神经,雷诺嗪,心肌梗塞,NE,BNP,促炎症。
Current Molecular Medicine
Title:Vagal Stimulation Facilitates Improving Effects of Ranolazine on Cardiac Function in Rats with Chronic Ischemic Heart Failure
Volume: 18 Issue: 1
关键词: 迷走神经,雷诺嗪,心肌梗塞,NE,BNP,促炎症。
摘要: Background: Ranolazine is generally used to treat anginal symptoms for patients with symptomatic chronic stable angina pectoris. By improving ischemiareperfusion, ranolazine is also observed to have protective effects on myocardial ischemic injury in animal models. It is noteworthy to find interventions that can decrease adverse effects of this drug and thereby increase its clinical application.
Methods: In this report, we used a rat model of chronic ischemic heart failure (CHF) to examine if vagal stimulation can strengthen the effects of ranolazine on worsened cardiac function in CHF. Plasma norepinephrine (NE) and brain natriuretic peptide [BNP, termed B-type natriuretic peptide-45 (BNP-45) in rats] are regulated by sympathetic nerve activity. Because NE and BNP are considered as neurohormones indicating heart failure progression, we also determined the levels of plasma NE and BNP-45 besides cardiac function. Moreover, we examined the role of sympathetic pro-inflammatory cytokines in engagement of vagal activation.
Results: Our data show that ranolazine intraperitoneally improved the impaired left ventricular function, and attenuated the exaggerated NE/BNP-45 and cytokines (such as IL-1β, IL-6 and TNF-α) after development of CHF. Particularly, our results show that vagal activation largely amplified the effects of ranolazine on cardiac function in CHF.
Conclusion: Our data indicate that: 1) ranolazine alleviates sympathetic nerve activity thereby leading to improvement of the worsened cardiac function in CHF; and 2) vagal stimulation augments the effect of ranolazine. Accordingly, results of this study have implications for the role played by a combination of vagal stimulation and ranolazine in improving cardiac function in CHF.
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Cite this article as:
Vagal Stimulation Facilitates Improving Effects of Ranolazine on Cardiac Function in Rats with Chronic Ischemic Heart Failure, Current Molecular Medicine 2018; 18 (1) . https://dx.doi.org/10.2174/1566524018666180608085330
DOI https://dx.doi.org/10.2174/1566524018666180608085330 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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