Plasma Adrenaline and Noradrenaline in Patients with Acute Myocardial Infarction

Bertel, Osmund; Bühler, Fritz R.; Baitsch, G; Ritz, R; Burkart, F

doi:10.1378/chest.82.1.64

Cited by 76 publications

(19 citation statements)

References 23 publications

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“…On the other hand, a large amount of data suggest the importance of an efficient production of cathecolamines in healthy aging and longevity. Indeed, there are now numerous studies demonstrating that sympathetic factors play a central role not only in cardiovascular homeostatic control, but also in pathogenesis and/or in the progression of several cardiovascular diseases, such as essential hypertension (Rahn et al, 1999) and myocardial infarction (Bertel et al, 1982). Therefore, a good efficiency in TH gene transcription may be a key for an appropriate response towards stochastic and age-related stress factors, and consequently for longevity.…”

Section: Discussionmentioning

confidence: 99%

The influences on human longevity by HUMTHO1.STR polymorphism (Tyrosine Hydroxylase gene)

Tan

Bellizzi

Rose

et al. 2002

Mechanisms of Ageing and Development

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A new method based on the recently developed relative risk approach is introduced, and applied to data from Italian centenarian study (965 subjects aged from 13 to 109 years old) for investigating influences on longevity by Tyrosine Hydroxylase (TH) gene variability. The strategic parameterization enables the model to disentangle the various ways by which HUMTHO1.STR alleles (alleles 6, 7, 8, 9, 10*, 10, as defined according to the number of repeats) may contribute in reducing or increasing the hazard of death with different patterns of influences. Among all the alleles, we have found that allele 10* (10 imperfect repeats) shows a remarkable dominant and beneficial effect that reduces the log hazard of death in an additive manner. The results confirm that HUMTHO1.STR polymorphism is involved in the modulation of human longevity. #

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Section: Discussionmentioning

confidence: 99%

The influences on human longevity by HUMTHO1.STR polymorphism (Tyrosine Hydroxylase gene)

Tan

Bellizzi

Rose

et al. 2002

Mechanisms of Ageing and Development

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“…This potentiation of I K-ATP activation by isoproterenol may underlie the effect of catecholamines to increase the risk of life-threatening arrhythmias under ischemic conditions and may contribute to the protective effect of ␤-blockers. 26,27 The I Kr blocker E4031 partially reversed the effect of pinacidil. pVT could still be induced at a BCL of 2000 ms in 1 preparation and at a BCL of 600 ms in 2 additional preparations.…”

Section: Circulation December 14 2004mentioning

confidence: 98%

Amplified Transmural Dispersion of Repolarization as the Basis for Arrhythmogenesis in a Canine Ventricular-Wedge Model of Short-QT Syndrome

2004

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Background-The short-QT syndrome is a new clinical entity characterized by corrected QT intervals Ͻ300 ms and a high incidence of ventricular tachycardia (VT) and fibrillation (VF). Gain-of-function mutations in the gene for outward potassium currents have been shown to underlie the congenital syndrome. The present study examined the cellular basis of VT/VF in an experimental model associated with short QT intervals created with a potassium channel activator. Methods and Results-Transmembrane action potentials from epicardial and M regions, 4 transmural unipolar electrograms, and a pseudo-ECG were simultaneously recorded in canine arterially perfused left ventricular wedge preparations. At a basic cycle length of 2000 ms, pinacidil (2 to 3 mol/L) abbreviated the QT interval from 303.7Ϯ5.4 to 247.3Ϯ6.9 ms (meanϮSEM, PϽ0.0001). The maximal transmural dispersion of repolarization (TDR max ) increased from 27.0Ϯ3.8 to 64.9Ϯ9.2 ms (PϽ0.01), and an S2 applied to the endocardium induced a polymorphic VT (pVT) in 9 of 12 wedge preparations (PϽ0.01). Addition of isoproterenol (100 nmol/L, nϭ5) led to greater abbreviation of the QT interval, a further increase in TDR max (from 55.4Ϯ13.7 to 69.7Ϯ8.3 ms), and more enduring pVT. TDR max was correlated significantly with the T peak -T end interval under all conditions. The effects of pinacidil were completely reversed by glybenclamide (10 mol/L, nϭ4) and partially reversed by E4031 (5 mol/L, nϭ5), which prevented induction of pVT in 3 of 5 preparations. Conclusions-Our

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“…Epinephrine alone can be arrhythmogenic [27,28]. Epinephrine enhances automaticity, lowers fibrillation thresholds [17,18,27,29,30] and increases extrasystoles [28,31].…”

Section: Epinephrine and Arrhythmic Riskmentioning

confidence: 99%

“…Epinephrine enhances automaticity, lowers fibrillation thresholds [17,18,27,29,30] and increases extrasystoles [28,31]. The effects on the action potential vary, but epinephrine alters calcium handling and increases the likelihood of delayed after-depolarizations [32][33][34][35].…”

Section: Epinephrine and Arrhythmic Riskmentioning

confidence: 99%

A possible mechanism of halocarbon-induced cardiac sensitization arrhythmias

Jing

Jesús

Iravanian

et al. 2006

Journal of Molecular and Cellular Cardiology

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Cardiac sensitization is the term used for malignant ventricular arrhythmias associated with exposure to inhaled halocarbons in the presence of catecholamines. We investigated the electrophysiological changes associated with cardiomyocyte exposure to epinephrine and a halocarbon known to be associated with cardiac sensitization (halon 1301, CF 3 Br). Cardiomyocytes (CMs) were isolated from neonatal rats and grown on multielectrode arrays (MEAs). Upon exposure to epinephrine, the CM inter-spike interval (ISI) was decreased 14% at 10 µg/L (P<0.05) and 27% at 100 µg/L (P<0.05) as compared to baseline. Halon alone (50 mg/L) mildly prolonged the field potential (FP) duration (7%). CMs exposed to combinations of epinephrine (100 µg/L) and halon (50 mg/L) for 15 min showed a blunted increase in the ISI (35±12%) and a 38% decrease in conduction velocity (P<0.05) when compared to epinephrine alone. There was no change in field potential properties, but dephosphorylated connexin 43 (Cx43) was increased 60±16% with the combination as compared to epinephrine alone (P<0.05). Treatment with okadaic acid, a phosphatase inhibitor, prevented the Cx43 dephosphorylation and the reduction in conduction velocity upon exposure to halon and epinephrine. Moreover, the electrophysiological changes induced by epinephrine and halon were indistinguishable from those seen with the gap junction inhibitor heptanol. In conclusion, the combination of a halocarbon and epinephrine results in a unique electrophysiological signature including slow conduction that may explain, in part, the basis for cardiac sensitization. The slowing of conduction is most likely related to changes in the phosphorylation state of Cx43.

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Plasma Adrenaline and Noradrenaline in Patients with Acute Myocardial Infarction

Cited by 76 publications

References 23 publications

The influences on human longevity by HUMTHO1.STR polymorphism (Tyrosine Hydroxylase gene)

The influences on human longevity by HUMTHO1.STR polymorphism (Tyrosine Hydroxylase gene)

Amplified Transmural Dispersion of Repolarization as the Basis for Arrhythmogenesis in a Canine Ventricular-Wedge Model of Short-QT Syndrome

A possible mechanism of halocarbon-induced cardiac sensitization arrhythmias

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