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Prevention of cell swelling with low chloride St. Thomas' Hospital solution improves postischemic myocardial recovery
A M Jayawant1, E R Stephenson, C M Baumgarten
1Department of Surgery, The Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
Insights
Lowering chloride in St. Thomas
Area of Science:
- Cardiology
- Cardiovascular Surgery
- Biochemistry
Background:
- Cardioplegia-induced cell swelling is a known issue in cardiac surgery.
- Previous studies in isolated myocytes suggest impermeant ion substitution can prevent swelling.
Purpose of the Study:
- To test if substituting chloride (Cl-) in St. Thomas' Hospital cardioplegic solution improves myocardial protection in blood-perfused hearts.
- To evaluate the impact of reduced KCl product on cardiac function and electrophysiology.
Main Methods:
- A rabbit heart Langendorff model was used for hypothermic global ischemia and reperfusion.
- Hearts received either standard or low-Cl- St. Thomas' Hospital cardioplegia (isosmotic, single bolus).
- Chloride was replaced with methanesulfonate; postreperfusion function and conduction were assessed.
Main Results:
- Low-Cl- cardioplegia significantly improved postischemic functional recovery (74% vs. 55%).
- Atrioventricular conduction remained normal in the low-Cl- group, unlike the standard group.
Conclusions:
- Reducing the KCl product of St. Thomas' Hospital solution prevents cellular edema by making it isotonic.
- This modification ameliorates functional and electrophysiologic damage from hypothermic, hyperkalemic cardioplegia.
Objective:
In isolated myocytes cardioplegia-induced cell swelling can be prevented by lowering the KCl 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 degrees to 12 degrees 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 [CI-]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.