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Role of calcium desensitization in the treatment of myocardial dysfunction after deep hypothermic circulatory arrest

Rewarming from deep hypothermic circulatory arrest (DHCA) produces calcium desensitization by troponin I (cTnI) phosphorylation which results in myocardial dysfunction. This study investigated the acute overall hemodynamic and metabolic effects of epinephrine and levosimendan, a calcium sensitizer,...

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Published in:Critical care (London, England) England), 2013-10, Vol.17 (5), p.R245-R245, Article R245
Main Authors: Rungatscher, Alessio, Hallström, Seth, Giacomazzi, Alice, Linardi, Daniele, Milani, Elisabetta, Tessari, Maddalena, Luciani, Giovanni Battista, Scarabelli, Tiziano M, Mazzucco, Alessandro, Faggian, Giuseppe
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Language:English
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Summary:Rewarming from deep hypothermic circulatory arrest (DHCA) produces calcium desensitization by troponin I (cTnI) phosphorylation which results in myocardial dysfunction. This study investigated the acute overall hemodynamic and metabolic effects of epinephrine and levosimendan, a calcium sensitizer, on myocardial function after rewarming from DHCA. Forty male Wistar rats (400 to 500 g) underwent cardiopulmonary bypass (CPB) through central cannulation and were cooled to a core temperature of 13°C to 15°C within 30 minutes. After DHCA (20 minutes) and CPB-assisted rewarming (60 minutes) rats were randomly assigned to 60 minute intravenous infusion with levosimendan (0.2 μg/kg/min; n = 15), epinephrine (0.1 μg/kg/min; n = 15) or saline (control; n = 10). Systolic and diastolic functions were evaluated at different preloads with a conductance catheter. The slope of left ventricular end-systolic pressure volume relationship (Ees) and preload recruitable stroke work (PRSW) recovered significantly better with levosimendan compared to epinephrine (Ees: 85 ± 9% vs 51 ± 11%, P
ISSN:1364-8535
1466-609X
1364-8535
DOI:10.1186/cc13071