| Abstract | Background: Hearts donated after circulatory death may represent an additional donor source. The influx of sodium and calcium ions across the sarcolemma play a central role in the pathogenesis of ischemia-reperfusion injury; however, this process may be inhibited if the initial reperfusion solution is rendered hypocalcemic and acidic. We sought to determine the calcium concentration and pH of the initial reperfusion solution that yielded optimal functional recovery of hearts donated after circulatory death during ex vivo heart perfusion. Methods: Pigs were anesthetized, mechanical ventilation was discontinued, and a 15-minute standoff period was observed after circulatory arrest. Hearts were reperfused with a normothermic cardioplegia of varying calcium concentrations (part 1 [50 μmol/L, n = 4; 220 μmol/L, n = 9; 500 μmol/L, n = 4; and 1,250 μmol/L, n = 5]) and pH (part 2 [7.9, n = 5; 7.4, n = 9; 6.9, n = 8; and 6.4, n = 6]). Myocardial function was then assessed in a physiologic working model 1 hour after initiation of normothermic ex vivo heart perfusion. Results: The calcium concentration and pH of the cardioplegic solution affected the development of myocardial edema (part 1: 50 μmol/L = 5.8% ± 0.9%; 220 μmol/L = 4.3% ± 0.4%; 500 μmol/L = 7.0% ± 0.6%; and 1,250 μmol/L = 6.6% ± 0.8% weight gain, p = 0.015; part 2: 7.9 = 3.6% ± 0.4%, 7.4 = 4.3% ± 0.4%, 6.9 = 3.7% ± 0.6%, and 6.4 = 6.4% ± 1.3% weight gain, p = 0.056) and the recovery of myocardial function (cardiac index part 1: 50 μmol/L = 2.6 ± 0.6; 220 μmol/L = 6.0 ± 0.8; 500 μmol/L = 2.3 ± 0.5; and 1,250 μmol/L = 1.9 ± 0.6 mL · m−1 · g−1, p < 0.001; part 2: 7.9 = 1.5 ± 0.7; 7.4 = 6.0 ± 0.8; 6.9 = 8.4 ± 1.8; and 6.4 = 3.1 ± 0.8 mL · m−1 · g−1, p = 0.003) during ex vivo heart perfusion. Conclusions: Initial reperfusion of hearts donated after circulatory death with a hypocalcemic and moderately acidic cardioplegia minimizes edema and optimizes functional recovery during subsequent ex vivo heart perfusion. |
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