艾司洛尔激活内源性神经激肽活性,抑制大鼠梗死性心律失常:抗心律失常的新机制

Li-Li Wang , Yi Han , Zheng Guo , Shi-Qi Han , Tao Liu
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引用次数: 8

摘要

内源性神经激肽和肾上腺素能机制可能共同参与急性心肌梗死(MI)的病理过程。本研究旨在探讨内源性神经激肽在梗死性心律失常中的作用及其与β1-肾上腺素能机制的关系。心肌梗死后60min,检测心肌缺血危险部位神经激肽1受体(NK1-R)天然激动剂P物质(SP)、去甲肾上腺素(NE)、NK1-R、β1-肾上腺素受体)的含量,分析室性心律失常。研究了NK1-R特异性拮抗剂D-SP (152 ng/kg)、β1-肾上腺素能受体特异性阻滞剂艾司洛尔(10 mg/kg)预处理及两种阻滞剂联合用药的效果。结果表明,NE、SP的上调与室性心律失常的增加存在重叠。D-SP加重了VT的发作和持续时间;VF分别上涨54%和104% (P <0.05)。艾司洛尔降低了VT的发病率、发作次数和持续时间;VF分别提高66%、92%和95%。令人惊讶的是,在整个心肌梗死期间,艾司洛尔显著减弱了D-SP的致心律失常作用,超出了艾司洛尔作用的时间跨度,在此期间,NK1-R的显著上调(19%,P <0.05)。综上所述,本研究结果可能提示内源性神经激肽的抗心律失常作用机制,通过激活内源性神经激肽,通过上调NK1受体,艾司洛尔可能在急性心肌梗死早期发挥其抗心律失常作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Esmolol activates endogenous neurokinin activity inhibiting infarction-induced arrhythmias in rats: Novel mechanisms of anti-arrhythmia

Endogenous neurokinin and adrenergic mechanisms might co-participate in the pathology of acute myocardial infarction (MI). This study sought to investigate the role of endogenous neurokinin and its relationship with β1-adrenergic mechanism in the infarction induced arrhythmias.

In 60 min of MI in rats, the contents of substance P (SP), a native agonist of neurokinin 1 receptor (NK1-R), norepinephrine (NE), NK1-R and β1-adrenergic receptor in the myocardium at risk of ischemia were examined and the ventricular arrhythmias were analyzed. The effects of pretreatment with D-SP (152 ng/kg), a specific antagonist of NK1-R, esmolol (10 mg/kg), a specific blocker of β1-adrenergic receptor, and a combination of the two blockers were studied. The results showed that the overlaps of up-regulation of NE, SP and the increase of ventricular arrhythmias were observed. D-SP exacerbated the episodes and duration of VT & VF by 54% and 104%, respectively (all P < 0.05). Esmolol inhibited the morbidity rate, the episodes and the duration of VT & VF by 66%, 92% and 95%, respectively. Surprisingly, esmolol significantly attenuated the arrhythmogenic effect of D-SP throughout the MI, beyond the time span of esmolol action, during which a significant up-regulation of the NK1-R (by 19%, P < 0.05) was detected.

In conclusion, the findings of this study may indicate an anti-arrhythmic effect of endogenous neurokinin mechanism, through the activation of which, via up-regulation of NK1 receptor, esmolol may exert its anti-arrhythmic action at the early time of acute myocardial infarction.

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来源期刊
Regulatory Peptides
Regulatory Peptides 医学-内分泌学与代谢
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审稿时长
2 months
期刊介绍: Regulatory Peptides provides a medium for the rapid publication of interdisciplinary studies on the physiology and pathology of peptides of the gut, endocrine and nervous systems which regulate cell or tissue function. Articles emphasizing these objectives may be based on either fundamental or clinical observations obtained through the disciplines of morphology, cytochemistry, biochemistry, physiology, pathology, pharmacology or psychology.
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