Free radicals mediate postshock contractile impairment in cardiomyocytes

Min Shan Tsai; Shijie Sun; Wanchun Tang; Giuseppe Ristagno; Wen Jone Chen; Max Harry Weil

doi:10.1097/CCM.0b013e31818f23f0

Free radicals mediate postshock contractile impairment in cardiomyocytes

Min Shan Tsai, Shijie Sun, Wanchun Tang, Giuseppe Ristagno, Wen Jone Chen, Max Harry Weil

Istituto di Ricerche Farmacologiche "Mario Negri"

Research output: Contribution to journal › Article

Abstract

OBJECTIVE: Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups. MEASUREMENTS AND MAIN RESULTS: DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% ± 2.5% to 5.6% ± 3.4% (p = 0.000) and the Ca transient decreased from 1.15 ± 0.13 au to 1.08 ± 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca transient. CONCLUSION: Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.

Original language	English
Pages (from-to)	3213-3219
Number of pages	7
Journal	Critical Care Medicine
Volume	36
Issue number	12
DOIs	https://doi.org/10.1097/CCM.0b013e31818f23f0
Publication status	Published - Dec 2008

Keywords

Ascorbic acid
Cardiomyocytes
Electrical shock
Free radicals
Length shortening

ASJC Scopus subject areas

Critical Care and Intensive Care Medicine

Access to Document

10.1097/CCM.0b013e31818f23f0

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Tsai, M. S., Sun, S., Tang, W., Ristagno, G., Chen, W. J., & Weil, M. H. (2008). Free radicals mediate postshock contractile impairment in cardiomyocytes. Critical Care Medicine, 36(12), 3213-3219. https://doi.org/10.1097/CCM.0b013e31818f23f0

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title = "Free radicals mediate postshock contractile impairment in cardiomyocytes",

abstract = "OBJECTIVE: Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups. MEASUREMENTS AND MAIN RESULTS: DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% ± 2.5% to 5.6% ± 3.4% (p = 0.000) and the Ca transient decreased from 1.15 ± 0.13 au to 1.08 ± 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca transient. CONCLUSION: Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.",

keywords = "Ascorbic acid, Cardiomyocytes, Electrical shock, Free radicals, Length shortening",

author = "Tsai, {Min Shan} and Shijie Sun and Wanchun Tang and Giuseppe Ristagno and Chen, {Wen Jone} and Weil, {Max Harry}",

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T1 - Free radicals mediate postshock contractile impairment in cardiomyocytes

AU - Tsai, Min Shan

AU - Sun, Shijie

AU - Tang, Wanchun

AU - Ristagno, Giuseppe

AU - Chen, Wen Jone

AU - Weil, Max Harry

PY - 2008/12

Y1 - 2008/12

N2 - OBJECTIVE: Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups. MEASUREMENTS AND MAIN RESULTS: DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% ± 2.5% to 5.6% ± 3.4% (p = 0.000) and the Ca transient decreased from 1.15 ± 0.13 au to 1.08 ± 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca transient. CONCLUSION: Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.

AB - OBJECTIVE: Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock. DESIGN: Randomized prospective animal study. SETTING: University affiliated research laboratory. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups. MEASUREMENTS AND MAIN RESULTS: DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% ± 2.5% to 5.6% ± 3.4% (p = 0.000) and the Ca transient decreased from 1.15 ± 0.13 au to 1.08 ± 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca transient. CONCLUSION: Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.

KW - Ascorbic acid

KW - Cardiomyocytes

KW - Electrical shock

KW - Free radicals

KW - Length shortening

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