Acute electrophysiologic consequences of pyridostigmine inhibition of cholinesterase in humans

Zimerman, Leandro Ioschpe; Liberman, Alon; Castro, Renata Rodrigues Teixeira de; Ribeiro, Jorge Pinto; Nóbrega, Antônio Cláudio Lucas da

doi:10.1590/s0100-879x2010005000001

Cited by 9 publications

(11 citation statements)

References 35 publications

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“…59 Previous studies have reported that expression of Cx43 was decreased during hypoxia, 60 ischaemia, 59 MI, 61 and heart failure. 17,26 Similarly, an intervention with VNS was shown to preserve Cx43 in AMI rats. 65 Interestingly, pyridostigmine has been shown to protect hearts against ischaemia-induced arrhythmia by preserving Cx43 in AMI rats and preventing prolonging of a corrected QT (QTc) interval by reducing the refractory ventricular period, thereby reducing incidence of premature ventricular beats.…”

Section: Thus Prevented Ischaemia-induced Arrythmia In Ami Ratsmentioning

confidence: 95%

“…In contrast, vagal nerve rarely innervates the ventricles and less affects to negative inotropic effects. [15][16][17] Since cervical VNS is invasive and required a surgical procedure to implant this electrical device and could cause adverse events such as neck pain or coughing, these limit its clinical use. 13 Emerging evidence has demonstrated that modulation of vagal activity provided beneficial effects in CVDs.…”

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confidence: 99%

“…Direct activation of vagus nerve by electrical VNS have been shown to exert cardioprotection under various conditions. [15][16][17] Since cervical VNS is invasive and required a surgical procedure to implant this electrical device and could cause adverse events such as neck pain or coughing, these limit its clinical use. 18 Recent studies showed that non-invasive stimulation of the auricular branch of the vagus nerve by low-level tragus stimulation showed beneficial effects in CVDs in both animal 19,20 and clinical models.…”

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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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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: Thus Prevented Ischaemia-induced Arrythmia In Ami Ratsmentioning

confidence: 95%

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confidence: 99%

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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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“…The pharmacological enhancement of cholinergic activity to the heart using PYR also reduced the incidence of PVBs in patients with heart failure (5) and arrhythmias but no history of MI (59). Zimerman et al (65) suggested that the antiarrhythmic effect of PYR could be partially related to a reduction of the refractory ventricular period, which was shorter in humans after a single dose of PYR.…”

Section: Electrocardiographic Responsesmentioning

confidence: 99%

Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein

Santos-Almeida

Girão

Silva

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Fazan R Jr. Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein. Am J Physiol Heart Circ Physiol 308: H101-H107, 2015. First published November 21, 2014; doi:10.1152/ajpheart.00591.2014.-We investigated the effects of acute pyridostigmine (PYR) treatment, an acetylcholinesterase inhibitor, on arterial pressure (AP), heart rate (HR), cardiac sympathovagal balance, and the incidence of arrhythmias during the first 4 h after myocardial infarction (MI) in anesthetized rats. Male Wistar rats were implanted with catheters into the femoral artery and vein for AP recordings and drug administration. Rats received the autonomic receptor blockers methyl-atropine (1 mg/kg iv) and propranolol (2 mg/kg iv) at intervals of 15 min, 1 h after saline (n ϭ 16) or PYR (0.25 mg/kg iv, n ϭ 18), to indirectly assess sympathovagal balance. Acute treatment with PYR increased cardiac vagal (86 Ϯ 7 vs. 44 Ϯ 5 beats/min) and decreased sympathetic tone (Ϫ31 Ϯ 8 vs. Ϫ69 Ϯ 7 beats/min). Different animals were implanted with ECG electrodes and catheters. A large MI was induced via left coronary artery ligation after basal recordings. Rats received PYR (n ϭ 14) or saline (n ϭ 14) 10 -15 min after MI, and the recordings lasted up to 4 h. In part of the animals, hearts were removed for connexin43 quantification after all procedures. MI elicited a fall in AP (Ϫ45 Ϯ 5 mmHg), a progressive rise in HR (26 Ϯ 14 beats/min), and an increase in corrected QT interval (33 Ϯ 13 ms). PYR elicited a prompt bradycardia (Ϫ50 Ϯ 14 beats/min) that returned to basal levels over time, and it prevented the lengthening of the corrected QT interval. Treatment with PYR increased by ϳ20% the occurrence of rats free of arrhythmias after MI. MI markedly decreased connexin43 in left ventricles, and PYR treatment partially prevented this decrease. parasympathetic stimulation; anticholinesterase agent; myocardial infarction; autonomic imbalance; arrhythmias MYOCARDIAL INFARCTION (MI) is a key component of the burden of cardiovascular disease and one of the leading causes of death in high-or middle-income countries (49, 61). Epidemiological evidence establishes that 50% of MI patients do not survive the first hour after MI before receiving any medical support (37) and that ventricular arrhythmia causes most of these deaths (60). These observations are corroborated by experiments in animal models of MI (25,28,44). Myocardial ischemia and MI are often accompanied by a marked autonomic imbalance that is characterized by sympathetic overactivity (38, 60) and vagal attenuation (54).

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“…Pyridostigmine bromide, an anticholinesterasic agent that has been used for many years to treat myasthenia gravis , exhibits protective cardiovascular effects during short-term administration that lead to a reduction of cardiovascular risk markers and an improvement of autonomic dysfunction [26, 26, 27, 27–29]. By potentiating vagal parasympathetic function, this compound is thought to provoke sinus bradycardia, to reduce AV nodal conduction and the refractory period of action potentials and to increase the cardiac excitation threshold, among other direct cardiac effects.…”

Section: Introductionmentioning

confidence: 99%

Effects of Cholinergic Stimulation with Pyridostigmine Bromide on Chronic Chagasic Cardiomyopathic Mice

Cuba

Machado

Farnesi

et al. 2014

Mediators of Inflammation

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The aim of the present study was to assess the effects of an anticholinesterase agent, pyridostigmine bromide (Pyrido), on experimental chronic Chagas heart disease in mice. To this end, male C57BL/6J mice noninfected (control:Con) or chronically infected (5 months) with Trypanosoma cruzi (chagasic:Chg) were treated or not (NT) with Pyrido for one month. At the end of this period, electrocardiogram (ECG); cardiac autonomic function; heart histopathology; serum cytokines; and the presence of blood and tissue parasites by means of immunohistochemistry and PCR were assessed. In NT-Chg mice, significant changes in the electrocardiographic, autonomic, and cardiac histopathological profiles were observed confirming a chronic inflammatory response. Treatment with Pyrido in Chagasic mice caused a significant reduction of myocardial inflammatory infiltration, fibrosis, and hypertrophy, which was accompanied by a decrease in serum levels of IFNγ with no change in IL-10 levels, suggesting a shift of immune response toward an anti-inflammatory profile. Lower nondifferent numbers of parasite DNA copies were observed in both treated and nontreated chagasic mice. In conclusion, our findings confirm the marked neuroimmunomodulatory role played by the parasympathetic autonomic nervous system in the evolution of the inflammatory-immune response to T. cruzi during experimental chronic Chagas heart disease in mice.

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Acute electrophysiologic consequences of pyridostigmine inhibition of cholinesterase in humans

Cited by 9 publications

References 35 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

Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein

Effects of Cholinergic Stimulation with Pyridostigmine Bromide on Chronic Chagasic Cardiomyopathic Mice

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