Impact of exercise training associated to pyridostigmine treatment on autonomic function and inflammatory profile after myocardial infarction in rats

Feriani, Daniele Jardim; Souza, Gabriel I.H.; Carrozzi, N.; Mostarda, Cristiano Teixeira; Dourado, Paulo Magno Martins; Consolim‐Colombo, Fernanda Marciano; Angelis, Kátia De; Moreno, Heitor; Irigoyen, Maria Cláudia; Rodrigues, Bruno

doi:10.1016/j.ijcard.2016.10.061

Cited by 24 publications

(52 citation statements)

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“…53 Several studies reported that AChE inhibitors suppress neurohumoral activation and sympathetic tone, thus improving cardiac autonomic function and cardiac remodelling in MI rats. 28,30,31,36,38,56 Similarly, pyridostigmine increased baroreflex sensitivity in MI rats. It has been shown that the high frequency (HF) component is a marker of parasympathetic tone, whereas the low frequency (LF) component is considered a marker of sympathetic and parasympathetic activity.…”

Section: Of 24mentioning

confidence: 91%

“…31,33,35,37,38 ACh from cholinergic nerve ending inhibits noradrenaline release by activation of muscarinic receptors near presynaptic sympathetic nerve terminals, thereby attenuating sympathetic activity. 14 Use of an AChE inhibitor has been shown to improve cardiac autonomic balance by increasing parasympathetic tone and suppressing sympathetic tone in rats with MI.…”

Section: Of 24mentioning

confidence: 99%

“…13,36,[54][55][56] Heart rate variability is an indirect method that is used to determine cardiac autonomic function. 31,35,37,38,56 All these reported benefits could contribute to attenuating the severity of MI. 57 AChE inhibitors increased the HF component, while decreasing the LF and LF/ HF ratio.…”

Section: Of 24mentioning

confidence: 99%

“…103 In the same way, donepezil enhanced the survival pathway through increasing the pAkt/Akt ratio, leading to improved cardiac function and survival of chronic heart failure mice. 27,31,32,37,38 However, there are inconsistencies as some reports demonstrate that AChE inhibitors may not attenuate infarct size after MI. 105 As infarct size plays an important role in cardiac remodelling and function, 106 it is promising that AChE inhibitors have been shown to attenuate infarct size and cardiac dysfunction in various models.…”

Section: F I G U R E 3 Schematic Representation Of the Possible Mechamentioning

confidence: 99%

“…21 However, further clinical studies are needed to warrant its clinical use. [26][27][28][29][30][31][32][33][34][35][36][37][38][39] Despite its potential clinical benefits for CVDs patients, the role of AChE inhibitors in AMI and heart failure remediation remains unclear. 22,23 Use of AChE inhibitors is a non-invasive intervention which increases the parasympathetic activity.…”

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The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

2019

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Cardiovascular diseases remain a major cause of morbidity and mortality worldwide. Cardiovascular diseases such as acute myocardial infarction, ischaemia/reperfusion injury and heart failure are associated with cardiac autonomic imbalance characterized by sympathetic overactivity and parasympathetic withdrawal from the heart. Increased parasympathetic activity by electrical vagal nerve stimulation has been shown to provide beneficial effects in the case of cardiovascular diseases in both animals and patients by improving autonomic function, cardiac remodelling and mitochondrial function. However, clinical limitations for electrical vagal nerve stimulation exist because of its invasive nature, costly equipment and limited clinical validation. Therefore, novel therapeutic approaches which moderate parasympathetic activities could be beneficial for in the case of cardiovascular disease. Acetylcholinesterase inhibitors inhibit acetylcholinesterase and hence increase cholinergic transmission. Recent studies have reported that acetylcholinesterase inhibitors improve autonomic function and cardiac function in cardiovascular disease models. Despite its potential clinical benefits for cardiovascular disease patients, the role of acetylcholinesterase inhibitors in acute myocardial infarction and heart failure remediation remains unclear. This article comprehensively reviews the effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure scenarios from in vitro and in vivo studies to clinical reports. The mechanisms involved are also discussed in this review.

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Section: Of 24mentioning

confidence: 99%

Section: Of 24mentioning

confidence: 99%

Section: F I G U R E 3 Schematic Representation Of the Possible Mechamentioning

confidence: 99%

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The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

2019

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Aerobic training prevents cardiometabolic changes triggered by myocardial infarction in ovariectomized rats

Ruberti

Sousa

Viana

et al. 2020

Journal Cellular Physiology

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This study aimed to evaluate the impact of aerobic training (AT) on autonomic, cardiometabolic, ubiquitin-proteasome activity, and inflammatory changes evoked by myocardial infarction (MI) in ovariectomized rats. Female Wistar rats were ovariectomized and divided into four groups: sedentary + sham (SS), sedentary + MI (SI), AT + sham surgery (TS), AT + MI (TI). AT was performed on a treadmill for 8 weeks before MI. Infarcted rats previously subjected to AT presented improved physical capacity, increased interleukin-10, and decreased pro-inflammatory cytokines. Metabolomic analysis identified and quantified 62 metabolites, 9 were considered significant by the Vip Score. SS, SI, and TS groups presented distinct metabolic profiles; however, TI could not be distinguished from the SS group. MI dramatically increased levels of dimethylamine, and AT prevented this response. Our findings suggest that AT may be useful in preventing the negative changes in functional, inflammatory, and metabolic parameters related to MI in ovariectomized rats.

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Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases

Liu

Zhao

et al. 2018

Neurosci. Bull.

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Cardiovascular diseases are life-threatening illnesses with high morbidity and mortality. Suppressed vagal (parasympathetic) activity and increased sympathetic activity are involved in these diseases. Currently, pharmacological interventions primarily aim to inhibit over-excitation of sympathetic nerves, while vagal modulation has been largely neglected. Many studies have demonstrated that increased vagal activity reduces cardiovascular risk factors in both animal models and human patients. Therefore, the improvement of vagal activity may be an alternate approach for the treatment of cardiovascular diseases. However, drugs used for vagus nerve activation in cardiovascular diseases are limited in the clinic. In this review, we provide an overview of the potential drug targets for modulating vagal nerve activation, including muscarinic, and β-adrenergic receptors. In addition, vagomimetic drugs (such as choline, acetylcholine, and pyridostigmine) and the mechanism underlying their cardiovascular protective effects are also discussed.

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Impact of exercise training associated to pyridostigmine treatment on autonomic function and inflammatory profile after myocardial infarction in rats

Cited by 24 publications

References 46 publications

The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

The effects of acetylcholinesterase inhibitors on the heart in acute myocardial infarction and heart failure: From cells to patient reports

Aerobic training prevents cardiometabolic changes triggered by myocardial infarction in ovariectomized rats

Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases

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