Element concentrations (selenium, copper, zinc, iron, magnesium, potassium, phosphorous) in heart tissue of patients with coronary heart disease correlated with physiological parameters of the heart

Oster, O.; Dahm, Manfred; Oelert, H

doi:10.1093/eurheartj/14.6.770

Cited by 47 publications

(30 citation statements)

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“…Cardiac zinc content correlates positively with ejection fraction (EF) in humans (18), and zinc supplementation to cardioplegic solution protects against the loss of systolic function and enhances diastolic function during and after ischemia-reperfusion injury (23)(24)(25). It has been suggested that zinc combats oxidative stress associated with ischemia-reperfusion and diabetes in part by enhancing the capacity of the zinc-binding protein metallothionein (15), which shields against reactive oxygen species (13, 23-25, 27, 36).…”

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confidence: 99%

Identifying cellular mechanisms of zinc-induced relaxation in isolated cardiomyocytes

Vick

Vecchio

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Yi T, Vick JS, Vecchio MJ, Begin KJ, Bell SP, Delay RJ, Palmer BM. Identifying cellular mechanisms of zinc-induced relaxation in isolated cardiomyocytes. Am J Physiol Heart Circ Physiol 305: H706-H715, 2013. First published June 28, 2013 doi:10.1152/ajpheart.00025.2013.-We tested several molecular and cellular mechanisms of cardiomyocyte contraction-relaxation function that could account for the reduced systolic and enhanced diastolic function observed with exposure to extracellular Zn 2ϩ . Contraction-relaxation function was monitored in isolated rat and mouse cardiomyocytes maintained at 37°C, stimulated at 2 or 6 Hz, and exposed to 32 M Zn 2ϩ or vehicle. Intracellular Zn 2ϩ detected using FluoZin-3 rose to a concentration of ϳ13 nM in 3-5 min. Peak sarcomere shortening was significantly reduced and diastolic sarcomere length was elongated after Zn 2ϩ exposure. Peak intracellular Ca 2ϩ detected by Fura-2FF was reduced after Zn 2ϩ exposure. However, the rate of cytosolic Ca 2ϩ decline reflecting sarcoplasmic reticulum (SR) Ca 2ϩ -ATPase (SERCA2a) activity and the rate of Na ϩ /Ca 2ϩ exchanger activity evaluated by rapid Na ϩ -induced Ca 2ϩ efflux were unchanged by Zn 2ϩ exposure. SR Ca 2ϩ load evaluated by rapid caffeine exposure was reduced by ϳ50%, and L-type calcium channel inward current measured by whole cell patch clamp was reduced by ϳ70% in cardiomyocytes exposed to Zn 2ϩ . Furthermore, ryanodine receptor (RyR) S2808 and phospholamban (PLB) S16/T17 were markedly dephosphorylated after perfusing hearts with 50 M Zn 2ϩ . Maximum tension development and thinfilament Ca 2ϩ sensitivity in chemically skinned cardiac muscle strips were not affected by Zn 2ϩ exposure. These findings suggest that Zn 2ϩ suppresses cardiomyocyte systolic function and enhances relaxation function by lowering systolic and diastolic intracellular Ca 2ϩ concentrations due to a combination of competitive inhibition of Ca 2ϩ influx through the L-type calcium channel, reduction of SR Ca 2ϩ load resulting from phospholamban dephosphorylation, and lowered SR Ca 2ϩ leak via RyR dephosphorylation. The use of the low-Ca 2ϩ -affinity Fura-2FF likely prevented the detection of changes in diastolic Ca 2ϩ and SERCA2a function. Other strategies to detect diastolic Ca 2ϩ in the presence of Zn 2ϩ are essential for future work.cardiac; myocyte; sarcomere; L-type channel; ryanodine receptor THE IMPORTANCE of zinc and zinc ion (Zn 2ϩ ) in cardiac muscle function is only partially understood at this time. Cardiac zinc content correlates positively with ejection fraction (EF) in humans (18), and zinc supplementation to cardioplegic solution protects against the loss of systolic function and enhances diastolic function during and after ischemia-reperfusion injury (23-25). It has been suggested that zinc combats oxidative stress associated with ischemia-reperfusion and diabetes in part by enhancing the capacity of the zinc-binding protein metallothionein (15), which shields against reactive oxygen species (13, 23-25, 27, 36).Zinc deficiency (Ͻ10.7 M plasm...

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confidence: 99%

Identifying cellular mechanisms of zinc-induced relaxation in isolated cardiomyocytes

Vick

Vecchio

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…Also, in such patients, the myocardial tissue concentrations of these micronutrients showed positive correlations with cardiac output parameters [50,51] As stated before, arterial hypertension is accompanied by changes in zinc metabolism and its redistribution that may lead, at least, to zinc deficiency [52]. In turn, zinc deficiency may impair myocardial compensatory and reconstructive processes on increased left ventricular load and finally lead to left ventricular failure.…”

Section: Discussionmentioning

confidence: 66%

Selected Zinc Metabolism Parameters and Left Ventricle Mass in Echocardiographic Examination in Primary Arterial Hypertension

Tubek

2007

Biol Trace Elem Res

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The basal systolic and diastolic blood pressure, body mass index, left ventricular mass, serum and lymphocyte zinc levels, serum aldosterone, plasma rennin and angiotensin-converting enzyme activities, sodium and potassium levels, and the total and ouabain-dependent rate constants of zinc efflux from lymphocytes were measured in a group of 41 individuals of both sexes (overall age 46.3 +/- 11.4 years), of which 18 were women (48.5 +/- 7.1 years old) and 23 were men (44.7 +/- 13.8 years old). There were no significant differences between these parameters while dividing the subjects into groups according to sex, despite differences in weight, left ventricle mass, plasma rennin activity, and serum aldosterone content. Only the total and ouabain-dependent rate constants of zinc efflux from lymphocytes slightly negatively correlated to left ventricular mass, r = -0.30 to r = -0.36. This may constitute indirect evidence of zinc deficiency in cardiomyocytes of some hypertensive individuals with left ventricular hypertrophy.

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“…Oster et al (89) found a positive correlation between cardiac output and copper in heart tissue of patients with coronary heart disease (in addition to the similar correlation with selenium noted in Subheading 3). Copper deficient rats resemble those deficient in selenium in some aspects of selenium metabolism (71).…”

Section: Ischemic Heart Disease Resembles Copper Deficiencymentioning

confidence: 62%

Trace Element and Mineral Nutrition in Ischemic Heart Disease

Klevay¹

2000

Clinical Nutrition of the Essential Trace Elements and Minerals

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Element concentrations (selenium, copper, zinc, iron, magnesium, potassium, phosphorous) in heart tissue of patients with coronary heart disease correlated with physiological parameters of the heart

Cited by 47 publications

References 0 publications

Identifying cellular mechanisms of zinc-induced relaxation in isolated cardiomyocytes

Identifying cellular mechanisms of zinc-induced relaxation in isolated cardiomyocytes

Selected Zinc Metabolism Parameters and Left Ventricle Mass in Echocardiographic Examination in Primary Arterial Hypertension

Trace Element and Mineral Nutrition in Ischemic Heart Disease

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