Acute sleep deprivation (ASD) and cardioprotection: Impact of ASD on oxytocin-mediated sympathetic nervous activation preceding myocardial infarction

IF 2.5 3区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Marjan Aghajani , Mozhgan Aghajani , Ehsan Kazemi Moghaddam , Mahdieh Faghihi , Alireza Imani
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引用次数: 0

Abstract

Introduction

This study explored how acute sleep deprivation (ASD) before myocardial ischemia influences oxytocin release from paraventricular (PVN) neurons and its correlation with sympathetic nervous system (SNS) activity post-acute sleep loss, impacting subsequent left ventricular (LV) remodeling following myocardial infarction (MI).

Methods

The study was conducted in two phases: induction of ASD, inducing MI, blood sampling, euthanizing animals and collecting their heart and brain for histological and gene expression evaluations. The animals in first and second phase were euthanized 24 h and 14 days after MI, respectively.

Results

Pre-MI ASD, accompanied by increased serum epinephrine levels within 24 h of MI, upregulated oxytocin and cFos expression in the PVN. Also, pre-MI ASD resulted in decreased serum PAB levels 14 days post-MI (P < 0.001). While notable echocardiographic changes were seen in MI versus sham groups, ASD demonstrated protective effects. This was evidenced by reduced infarct size, elevated TIMP1, MMP2, and MMP9 in the LV of SD + MI animals versus MI alone (P < 0.05). Additionally, histological analysis showed reduced LV fibrosis in pre-MI ASD subjects (P < 0.05).

Conclusion

Our study supports the notion that activation of oxytocin neurons within the PVN subsequent to ASD interacts with autonomic centers in the central nervous system. This enhanced sympathetic outflow to the heart prior to MI triggers a preconditioning response, thereby mediating cardioprotection through decreased oxidative stress biomarkers and regulated extracellular matrix (ECM) turnover.

急性剥夺睡眠(ASD)与心脏保护:急性睡眠剥夺对心肌梗死前催产素介导的交感神经激活的影响。
简介:本研究探讨了心肌缺血前的急性睡眠剥夺(ASD)如何影响脑室旁(PVN)神经元的催产素释放及其与急性睡眠丧失后交感神经系统(SNS)活动的相关性,从而影响心肌梗死(MI)后的左心室重塑:研究分两个阶段进行:诱导 ASD、诱导心肌梗死、采血、安乐死动物并收集其心脏和大脑进行组织学和基因表达评估。第一和第二阶段的动物分别在心肌梗死后 24 小时和 14 天安乐死:结果:心肌梗死前ASD伴随着心肌梗死后24小时内血清肾上腺素水平的升高,上调了催产素和cFos在PVN中的表达。此外,心肌梗死前 ASD 导致心肌梗死后 14 天血清 PAB 水平下降(P 结论:我们的研究支持了心肌梗死前 ASD 激活催产素和 cFos 表达的观点:我们的研究支持这样一种观点,即 ASD 后催产素神经元在 PVN 内的激活与中枢神经系统的自律神经中枢相互作用。心肌梗死前交感神经向心脏外流的增强触发了预处理反应,从而通过减少氧化应激生物标志物和调节细胞外基质(ECM)的周转来介导心脏保护。
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来源期刊
Neuropeptides
Neuropeptides 医学-内分泌学与代谢
CiteScore
5.40
自引率
6.90%
发文量
55
审稿时长
>12 weeks
期刊介绍: The aim of Neuropeptides is the rapid publication of original research and review articles, dealing with the structure, distribution, actions and functions of peptides in the central and peripheral nervous systems. The explosion of research activity in this field has led to the identification of numerous naturally occurring endogenous peptides which act as neurotransmitters, neuromodulators, or trophic factors, to mediate nervous system functions. Increasing numbers of non-peptide ligands of neuropeptide receptors have been developed, which act as agonists or antagonists in peptidergic systems. The journal provides a unique opportunity of integrating the many disciplines involved in all neuropeptide research. The journal publishes articles on all aspects of the neuropeptide field, with particular emphasis on gene regulation of peptide expression, peptide receptor subtypes, transgenic and knockout mice with mutations in genes for neuropeptides and peptide receptors, neuroanatomy, physiology, behaviour, neurotrophic factors, preclinical drug evaluation, clinical studies, and clinical trials.
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