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J Thorac Cardiovasc Surg 1998;115:1196-1202
© 1998 Mosby, Inc.
CARDIOPULMONARY SUPPORT AND PHYSIOLOGY |
Supported by National Institutes of Health grants HL-51032 (R.J.D.),HL-09310 (A.M.J., R.J.D.), and HL-46764 (C.M.B.).
Received for publication April 25, 1997 Revisions requested Sept. 15, 1997. Revisions received Dec. 10, 1997 Accepted for publication Dec. 22, 1997. Address for reprints: Ralph J. Damiano, Jr., MD, Chief, Division ofCardiothoracic Surgery, The Milton S. Hershey Medical Center, Penn StateGeisinger Health System, P.O. Box 850, Hershey, PA 17033.
Objective: In isolated myocytescardioplegia-induced cell swelling can be prevented by lowering the KCl productby replacing Cl- with an impermeant ion. This study tested thehypothesis that Cl- substitution in St. Thomas' Hospitalcardioplegic solution would result in superior myocardial protection in theintact, blood-perfused heart.
Methods:Using a parabiotic, isolated rabbit heart Langendorff model, hearts were exposedto 1 hour of hypothermic (10° to 12° C), global ischemia followed by 30minutes of reperfusion. Isosmotic cardioplegia was administered as a single 50ml bolus of either standard St. Thomas' Hospital solution ([K+]ox [Cl-]o = 2566.4 (mmol/L)2) orlow Cl- St. Thomas' Hospital solution ([K+]ox [Cl-]o = 700 (mmol/L)2).Chloride was replaced by a large, impermeant ion, methanesulfonate.Postreperfusion systolic function and atrioventricular conduction times weremeasured before ischemia and after reperfusion.
Results:Hearts receiving low Cl St. Thomas' Hospital cardioplegia demonstratedsignificantly 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 Clgroup 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 ofhypothermic, hyperkalemic cardioplegia. (J Thorac Cardiovasc Surg1998;115:1196-202)
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