Modification of Epinephrine-induced Arrhythmias by N-Acetyl-L-Cysteine and Vitamin E

Sethi, Rajat; Adameová, Adriana; Dhalla, Ken S.; Khan, Mohsin; Elimban, Vijayan; Dhalla, Naranjan S.

doi:10.1177/1074248409333855

Cited by 24 publications

(34 citation statements)

References 33 publications

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“…The effects of intravenous cumulative doses of epinephrine (32 lg/kg) were also studied on plasma levels of catecholamines and MDA in control, vitamin A-and vitamin C-pretreated animals. This experimental design is similar to that used earlier [12,22]. The doses of epinephrine were selected in accordance with the previous experience with such experiments [12,23].…”

Section: Animal Model and Antioxidant Pretreatmentmentioning

confidence: 99%

“…On the other hand, epinephrine-induced arrhythmias have also been shown to occur through catecholamine oxidation products, aminochromes as well as the reactive oxygen species [11]. It is documented that epinephrine-induced arrhythmias were prevented by pretreating animals with antioxidants like N-acetyl-L-cysteine and vitamin E [12,13]. Another antioxidant, vitamin A has also been shown to exert antiarrhythmic effects [14], whereas alpha-tocopherol (vitamin E) has been reported to exert antiapoptotic actions [15].…”

Section: Introductionmentioning

confidence: 98%

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Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

et al. 2009

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Since excessive amounts of catecholamines are known to produce arrhythmias and increase the plasma level of aminochrome, an oxidation product of catecholamines, we tested the hypothesis that antioxidants may reduce the formation of aminochrome and prevent the catecholamine-induced arrhythmias. For this purpose, Sprague-Dawley rats were pretreated orally, with vitamin A or vitamin C for 21 days, and their effects on ventricular arrhythmias induced by a bolus dose or cumulative doses of intravenous epinephrine were examined. Electrocardiogram recording of these animals revealed that pretreatment with either of these vitamins increased the time of onset and decreased the duration of the epinephrine-induced ventricular arrhythmias. Ventricular fibrillations due to high doses of epinephrine were also prevented by the antioxidant pretreatment. Although pretreatment with either vitamin A or vitamin C did not affect the basal malondialdehyde level in control animals, the increase in malondialdehyde level caused by epinephrine administration was significantly reduced by these agents. The elevated level of plasma aminochrome due to epinephrine was also decreased by vitamins A and C treatments. The results indicate that antioxidant may prevent catecholamine-induced arrhythmias by reducing the formation of aminochrome and thus may provide a new strategy for the management of stress-related heart disease.

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Section: Animal Model and Antioxidant Pretreatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

et al. 2009

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“…These effects are mediated through the activation of β-adrenoceptors-cAMP-PKA system. Furthermore, in view of the occurrence of oxidative stress in diabetes (26,27,42), under conditions of increased catecholamines levels, there is an increase in the formation of catecholamine oxidation products, aminochromes, which have also been linked to arrhythmogenesis (2,3). Since the plasma levels of both Epi and NE were reduced in the 8-wk diabetic animals, there could also be a reduced production of aminochromes and therefore a reduced susceptibility to catecholamine-induced arrhythmias.…”

Section: Dose Of Epimentioning

confidence: 99%

“…The overactivation of the sympathetic nervous system is invariably seen in subjects with high risk for sudden cardiac death and elevated circulating catecholamine levels are considered to result in lethal ventricular arrhythmias and subsequent sudden cardiac death (1)(2)(3)(4). Such arrhythomogenic effects of catecholamines are generally believed to occur, in part, by producing defects in intracellular Ca 2+ -handling (1-4).…”

Section: Introductionmentioning

confidence: 99%

“…Such arrhythomogenic effects of catecholamines are generally believed to occur, in part, by producing defects in intracellular Ca 2+ -handling (1-4). In addition, oxyradicals, which are known to generate oxidative stress, may play a critical role in the genesis of ventricular arrhythmias that may result in sudden cardiac death (1)(2)(3)(4). Both bradycardia and malignant ventricular arrhythmias occur in diabetic subjects (5,6).…”

Section: Introductionmentioning

confidence: 99%

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Susceptibility of Diabetic Heart to Catecholamine-induced Arrhythmias is Independent of Contractile Dysfunction

Adameová

Elimban²,

Rodriguez-Leyva

et al. 2014

Serbian Journal of Experimental and Clinical Research

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Background: Diabetes is associated with myocardial electrical instability and prolongation of action potential duration that result in disturbances in the rhythm of the heart. Objective: Th is study was undertaken to examine the role of circulating catecholamines in abnormal cardiac rhythm and contractility during diff erent stages of diabetes. Methods: Diabetes was induced in male Sprague-Dawley rats with streptozotocin (STZ; 65 mg/kg, i.v.). Epinephrine (4-128 μg/kg, i.v.) -induced arrhythmias and plasma levels of epinephrine (Epi) and norepinephrine (NE) were determined in control, 4- and 8-wk diabetic animals. Echocardiography was used to assess cardiac remodeling and contractile function. Results: Although diabetes induced cardiac dysfunction, there were no significant differences in cardiac output, ejection fraction, left ventricle (LV) dimensions, LV fractional shortening between the 4- and 8-wk diabetic animals. Th e electrocardiogram of both diabetic groups showed deep S wave as well as changes in T wave and ST segment. In addition, prolongation of the RR interval in the 4- and 8-wk diabetic animals was seen, while prolongation of the QT and PR intervals were only seen in the 8-wk diabetic animals. Th e severity of Epi-induced ventricular arrhythmias, as assessed by arrhythmia score, was significantly lower in the 8-wk diabetic rats, as compared to the 4-wk diabetic animals. Circulating Epi levels were significantly decreased in the 8-wk diabetic rats, whereas NE levels were increased in the 4-wk diabetic rats. Conclusions: Th e sensitivity of the diabetic heart to catecholamine- triggered arrhythmias may be dependent on circulating Epi rather than NE and thus it can be proposed that the increased incidence of sudden cardiac death in diabetics may not be associated with response to catecholamines.

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Gender differences in β‐adrenoceptor system in cardiac hypertrophy due to arteriovenous fistula

Dent

Tappia

Dhalla

2010

Journal Cellular Physiology

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This study was undertaken to determine alterations in the β-adrenoceptor (β-AR) signaling system in male and female rats at 4 weeks after the induction of arteriovenous (AV) fistula or shunt. AV shunt produced a greater degree of cardiac hypertrophy and larger increase in cardiac output in male than in female animals. Increases in plasma levels of norepinephrine and epinephrine (EPI) due to AV shunt were also higher in male than females. While no difference in the β(1)-AR affinity was seen in males and females, AV shunt induced increase in β(1)-AR density in female rats was higher than that in males. Furthermore, no changes in basal adenylyl cyclase (AC) V/VI mRNA levels were seen; however, the increase in EPI-stimulated AC activities was greater in AV shunt females than in males. AV shunt decreased myocardial β(1)-AR mRNA level in male rats and increased β(2)-AR mRNA level in female hearts; an increase in G(i)-protein mRNA was detected only in male hearts. Although GRK2 gene expression was increased in both sexes, an increase in GRK3 mRNA was seen only in AV shunt female rats. β-arrestin1 mRNA was elevated in females whereas β-arrestin 2 gene expression was increased in both male and female AV shunt rats. While these data demonstrate gender associated differences in various components of the β-AR system in cardiac hypertrophy due to AV shunt, only higher levels of plasma catecholamines may account for the greater increase in cardiac output and higher degree of cardiac hypertrophy in males.

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Modification of Epinephrine-induced Arrhythmias by N-Acetyl-L-Cysteine and Vitamin E

Cited by 24 publications

References 33 publications

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

Susceptibility of Diabetic Heart to Catecholamine-induced Arrhythmias is Independent of Contractile Dysfunction

Gender differences in β‐adrenoceptor system in cardiac hypertrophy due to arteriovenous fistula

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