The Journal of Heart and Lung Transplantation, 2002
Objectives: Cardiac ischemia-reperfusion activates Na ϩ /H ϩ exchange; excess Na ϩ and the result... more Objectives: Cardiac ischemia-reperfusion activates Na ϩ /H ϩ exchange; excess Na ϩ and the resulting Ca 2ϩ overload, through reverse Na ϩ /Ca 2ϩ exchange, cause cellular injury and cardiac dysfunction. We postulated that inhibiting the Na ϩ /H ϩ isoform-1 exchanger would add to the protection of hearts after long-term cold storage in acidic cardioplegic solution. Methods: Guinea pig hearts were isolated and perfused at 37°C with Krebs-Ringer's solution (KRS) and then switched to an acidic St. Thomas solution (STS) at 25°C. Perfusion was stopped at 10°C, and hearts were stored for 6 hours in STS at 3.4°C. On reperfusion to 25°C, hearts were perfused with KRS for 60 minutes. Hearts were divided into 4 groups: sham control (SHAM); eniporide (EPR, EMD96785) IV, 1 mg/ kg given IV over 15 minutes before heart isolation; EPR intracoronary, 1 mol/liter in STS given intracoronary after heart isolation; and EPR IV and intracoronary. Results: Values at 60 minutes reperfusion (the percentage of control [100%] before cold storage) are given, respectively, for EPR IV, EPR intracoronary, and EPR IV and intracoronary vs drug-free SHAM (SEM, *p Ͻ 0.05 vs SHAM): 72% Ϯ 3%*, 65% Ϯ 3%*, and 81% Ϯ 2%* vs 55% Ϯ 3% for left ventricular pressure; 94% Ϯ 3%*, 96% Ϯ 5%*, and 102% Ϯ 2%* vs 81% Ϯ 3% for coronary flow; 60% Ϯ 2%, 58% Ϯ 3%, and 74%* Ϯ 3% vs 58% Ϯ 4% for cardiac efficiency; 106% Ϯ 2%*, 108% Ϯ 3%*, and 107% Ϯ 2%* vs 116% Ϯ 4% for percentage of O 2 extraction. Infarct size as percentage of ventricular weight was 20% Ϯ 3%*, 31% Ϯ 3%, and 6% Ϯ 2%* vs 35% Ϯ 3% (SHAM) after 60 minutes of reperfusion. Conclusions: Na ϩ /H ϩ isoform-1 exchanger inhibition, particularly if given IV before storage and intracoronary during cooling and rewarming, adds to the protection of cardioplegic solutions.
The Journal of Heart and Lung Transplantation, 2002
Objectives: Cardiac ischemia-reperfusion activates Na ϩ /H ϩ exchange; excess Na ϩ and the result... more Objectives: Cardiac ischemia-reperfusion activates Na ϩ /H ϩ exchange; excess Na ϩ and the resulting Ca 2ϩ overload, through reverse Na ϩ /Ca 2ϩ exchange, cause cellular injury and cardiac dysfunction. We postulated that inhibiting the Na ϩ /H ϩ isoform-1 exchanger would add to the protection of hearts after long-term cold storage in acidic cardioplegic solution. Methods: Guinea pig hearts were isolated and perfused at 37°C with Krebs-Ringer's solution (KRS) and then switched to an acidic St. Thomas solution (STS) at 25°C. Perfusion was stopped at 10°C, and hearts were stored for 6 hours in STS at 3.4°C. On reperfusion to 25°C, hearts were perfused with KRS for 60 minutes. Hearts were divided into 4 groups: sham control (SHAM); eniporide (EPR, EMD96785) IV, 1 mg/ kg given IV over 15 minutes before heart isolation; EPR intracoronary, 1 mol/liter in STS given intracoronary after heart isolation; and EPR IV and intracoronary. Results: Values at 60 minutes reperfusion (the percentage of control [100%] before cold storage) are given, respectively, for EPR IV, EPR intracoronary, and EPR IV and intracoronary vs drug-free SHAM (SEM, *p Ͻ 0.05 vs SHAM): 72% Ϯ 3%*, 65% Ϯ 3%*, and 81% Ϯ 2%* vs 55% Ϯ 3% for left ventricular pressure; 94% Ϯ 3%*, 96% Ϯ 5%*, and 102% Ϯ 2%* vs 81% Ϯ 3% for coronary flow; 60% Ϯ 2%, 58% Ϯ 3%, and 74%* Ϯ 3% vs 58% Ϯ 4% for cardiac efficiency; 106% Ϯ 2%*, 108% Ϯ 3%*, and 107% Ϯ 2%* vs 116% Ϯ 4% for percentage of O 2 extraction. Infarct size as percentage of ventricular weight was 20% Ϯ 3%*, 31% Ϯ 3%, and 6% Ϯ 2%* vs 35% Ϯ 3% (SHAM) after 60 minutes of reperfusion. Conclusions: Na ϩ /H ϩ isoform-1 exchanger inhibition, particularly if given IV before storage and intracoronary during cooling and rewarming, adds to the protection of cardioplegic solutions.
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Papers by Amadou Camara