Objective: In isolated myocytes cardioplegia-induced cell swelling can be prevented by lowering the KCI product by replacing Cl- with an impermeant ion. This study tested the hypothesis that Cl- substitution in St. Thomas' Hospital cardioplegic solution would result in superior myocardial protection in the intact, blood-perfused heart. Methods: Using a parabiotic, isolated rabbit heart Langendorff model, hearts were exposed to 1 hour of hypothermic (10°to 12°C), global ischemia followed by 30 minutes of reperfusion. Isosmotic cardioplegia was administered as a single 50 ml bolus of either standard St. Thomas' Hospital solution ([K+](o) x [Cl-](o) = 2566.4 (mmol/L)2) or low Cl- St. Thomas' Hospital solution ([K+](o) x [Cl-](o) = 700 (mmol/L)2). Chloride was replaced by a large, impermeant ion, methanesulfonate. Postreperfusion systolic function and atrioventricular conduction times were measured before ischemia and after reperfusion. Results: Hearts receiving low Cl- St. Thomas' Hospital cardioplegia demonstrated significantly better postischemic functional recovery (74% ± 3%) compared with those treated with standard high Cl- St. Thomas' Hospital solution (55% ± 4%, p = 0.003). In addition, atrioventricular conduction times remained normal in the low Cl- group but were significantly prolonged in the St. Thomas' Hospital group. Conclusions: Lowering the KCl product of St. Thomas' Hospital solution makes it isotonic with plasma and prevents cellular edema. This ameliorates the detrimental functional and electrophysiologic sequelae of hypothermic, hyperkalemic cardioplegia.
All Science Journal Classification (ASJC) codes
- Pulmonary and Respiratory Medicine
- Cardiology and Cardiovascular Medicine