Antiarrhythmic Effects of Magnesium on Rat Papillary Muscle and Guinea Pig Ventricular Myocytes

Aomine, Masahiro; Tatsukawa, Youichi; Yamato, Takako; Yamasaki, Satomi

doi:10.1016/s0306-3623(98)00094-9

Cited by 12 publications

(6 citation statements)

References 51 publications

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“…Magnesium therapy prevents recurrence of TdP without correction of the QT interval, even in patients with serum concentrations within the normal range (647). The underlying mechanism for the effectiveness of magnesium remains unclear, although one plausible hypothesis is that it suppresses EADs by blocking L-type calcium channels (27). Discontinued use of the suspected problematic medication appears an obvious concomitant step to alleviate TdP risk.…”

Section: Clinical Managementmentioning

confidence: 99%

hERG K⁺Channels: Structure, Function, and Clinical Significance

Vandenberg

Perry

Perrin

et al. 2012

Physiological Reviews

605

773

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The human ether-a-go-go related gene (hERG) encodes the pore-forming subunit of the rapid component of the delayed rectifier K(+) channel, Kv11.1, which are expressed in the heart, various brain regions, smooth muscle cells, endocrine cells, and a wide range of tumor cell lines. However, it is the role that Kv11.1 channels play in the heart that has been best characterized, for two main reasons. First, it is the gene product involved in chromosome 7-associated long QT syndrome (LQTS), an inherited disorder associated with a markedly increased risk of ventricular arrhythmias and sudden cardiac death. Second, blockade of Kv11.1, by a wide range of prescription medications, causes drug-induced QT prolongation with an increase in risk of sudden cardiac arrest. In the first part of this review, the properties of Kv11.1 channels, including biogenesis, trafficking, gating, and pharmacology are discussed, while the second part focuses on the pathophysiology of Kv11.1 channels.

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Section: Clinical Managementmentioning

confidence: 99%

hERG K⁺Channels: Structure, Function, and Clinical Significance

Vandenberg

Perry

Perrin

et al. 2012

Physiological Reviews

605

773

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“…Application of the CaMKII inhibitor KN93 led to similar results ( Figure 5, black bars). Mg 2+ has been shown to suppress both EADs and DADs in different models 26,27 and is used clinically as a first-line agent against TdP. Increasing extracellular [Mg 2+ ] from 1 mmol/L to 5 mmol/L abolished DADs induced after HMR1556 and ISO in 4 of 7 cells.…”

mentioning

confidence: 99%

Diastolic Spontaneous Calcium Release From the Sarcoplasmic Reticulum Increases Beat-to-Beat Variability of Repolarization in Canine Ventricular Myocytes After β-Adrenergic Stimulation

Johnson

Heijman

Bode

et al. 2013

Circulation Research

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2+ release (SCR) from the sarcoplasmic reticulum can cause delayed afterdepolarizations and triggered activity, contributing to arrhythmogenesis during β-adrenergic stimulation. Excessive beat-to-beat variability of repolarization duration (BVR) is a proarrhythmic marker. Previous research has shown that BVR is increased during intense β-adrenergic stimulation, leading to SCR.Objective: We aimed to determine ionic mechanisms controlling BVR under these conditions. potential (AP) of the single cardiac myocyte to the QT interval on the body surface. 7-9 Exaggerated BVR has been reported to be a more reliable indicator of arrhythmogenic risk than repolarization prolongation, per se, at least in several experimental ventricular tachycardia models [10][11][12] and in selected human subjects. 8,13 Although BVR has been investigated in multiple studies, the mechanisms underlying this phenomenon at the singlecell level remain to be fully elucidated. Pharmacological interventions influencing ion channels that operate during the AP plateau can markedly alter BVR. 7,14 Despite the fact that inhibition of the slowly activating delayed rectifier K + current (I Ks ) alone has minimal effects on both cellular AP duration (APD) and BVR, 14 we recently have shown that during increased Ca 2+ loading in myocytes subjected to blockade of I Ks in combination with βAR stimulation, BVR is significantly enhanced, even before the occurrence of EADs and TA. 14 In the present study, we investigated the relationship between SCR and BVR using a combined experimental and computational approach in both canine ventricular myocytes and in situ hearts subjected to βAR stimulation. We show that SCRs not only lead to I ti and DAD formation but also lead to a prolonged duration of AP via increased L-type Ca 2+ current (I CaL ), which in turn leads to increased BVR when analyzing multiple consecutive APs. Pharmacological interventions that inhibit SCR (either with reduced or with preserved systolic contraction) prevent this SCR-associated AP prolongation and reduce BVR. Methods and Results: MethodsThis investigation conformed to the Guide for the Care and Use of Laboratory Animals published by the United States National Institutes of Health (National Institutes of Health Publication 85-23, revised 1996). Animal handling was in accordance with the European Directive for the Protection of Vertebrate Animals Used for Experimental and Other Scientific Purposes (86/609/EU). Full details of methods, solutions, and interventions used are given in the onlineonly Data Supplement accompanying this article. A brief summary of the main aspects is provided. Myocyte Isolation and ElectrophysiologyCanine left ventricular (LV) myocytes were isolated as previously described. 15 Transmembrane APs were recorded at ≈37°C using highresistance (30-60 MΩ) glass microelectrodes filled with 3 mol/L KCl. Myocyte contractions were recorded with a video edge motion detector. Calcium MeasurementWe used the perforated patch-clamp technique under current-clamp or vol...

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“…The imbalance between the extracellular concentrations of Mg ++ and Ca ++ ions, as well as a prolonged calcium entry through L-type channels, would be involved in the genesis of vasospasm; in addition, the vasodilatory effect of MgSO 4 is reversed by calcium, while NO antagonists or prostanoids have no effect. The block of calcium channels, by an effect of competition with the Ca ++ ion, therefore seems to be the central point of the vascular effects of MgSO4, especially as the vasodilator effects of MgSO 4 are not dependent on the intracellular passage of the ion [3][4][5].…”

Section: Resultsmentioning

confidence: 99%

The Value of Magnesium Sulfate in the Pre-Hospital Phase of the Management of Eclampsia

Smiti¹,

Lamarti²,

Adnane³

2020

J Gynecol Res Rev Rep

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Eclampsia is a very serious complication of pregnancy, its occurrence is responsible of maternal and fetal morbidity and mortality. The aim of this study is to clarify the value of Magnesium Sulfate in the prevention of convulsive state and in the choice of anesthetic technique for cesarean section during eclampsia. We realized a prospective descriptive, analytical and comparative study over a period of 5 months, concerning a series of 49 pregnant women admitted to the anesthesia-intensive care unit of the Souissi Maternity Hospital in Rabat, with eclampsia. The diagnosis of eclampsia was made due to the occurrence of convulsive seizure (s) linked to pregnancy-induced hypertension. It was found that eclampsia mainly affected young women (age less than or equal to 25 years) with a percentage of 57.3%. The majority of patients were first-time mothers (55.1%). This condition manifests itself most often in the last trimester of pregnancy (72.9%), especially in pre-partum. The majority of patients did not receive an antenatal consultation. The treatment of choice in our study was magnesium sulfate. So, 51% of patients had not received magnesium sulfate before their admission to our hospital and 56% of them had had more than one seizure. And the 49% of patients, on the other hand, had received magnesium sulfate and only 18% of them had had the seizure again. Our obstetric attitude was based on immediate delivery with a caesarean section. 34.5% cesarean sections were performed under general anesthesia, compared with 65.5% under spinal anesthesia. The fetus morbidity was mainly represented by prematurity (30.6%) and neonatal distress (28.5%). The prognosis of eclampsia remains bleak both for the mother with a maternal mortality rate of 4%, and for the fetus with a perinatal mortality rate of 16.3%.

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Antiarrhythmic Effects of Magnesium on Rat Papillary Muscle and Guinea Pig Ventricular Myocytes

Cited by 12 publications

References 51 publications

hERG K⁺Channels: Structure, Function, and Clinical Significance

hERG K⁺Channels: Structure, Function, and Clinical Significance

Diastolic Spontaneous Calcium Release From the Sarcoplasmic Reticulum Increases Beat-to-Beat Variability of Repolarization in Canine Ventricular Myocytes After β-Adrenergic Stimulation

The Value of Magnesium Sulfate in the Pre-Hospital Phase of the Management of Eclampsia

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Antiarrhythmic Effects of Magnesium on Rat Papillary Muscle and Guinea Pig Ventricular Myocytes

Cited by 12 publications

References 51 publications

hERG K+Channels: Structure, Function, and Clinical Significance

hERG K+Channels: Structure, Function, and Clinical Significance

Diastolic Spontaneous Calcium Release From the Sarcoplasmic Reticulum Increases Beat-to-Beat Variability of Repolarization in Canine Ventricular Myocytes After β-Adrenergic Stimulation

The Value of Magnesium Sulfate in the Pre-Hospital Phase of the Management of Eclampsia

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hERG K⁺Channels: Structure, Function, and Clinical Significance

hERG K⁺Channels: Structure, Function, and Clinical Significance