Blood cardioplegia supplementation with the sodium-hydrogen ion exchange inhibitor cariporide to attenuate infarct size and coronary artery endothelial dysfunction after severe regional ischemia in a canine model
| Autor: | Cullen D. Morris, Jakob Vinten-Johansen, Satoshi Muraki, Zhi-Qing Zhao, Robert A. Guyton, Jason M Budde |
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| Rok vydání: | 2003 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine medicine.medical_specialty Sodium-Hydrogen Exchangers Endothelium Myocardial Infarction Ischemia Myocardial Reperfusion Injury Guanidines Neutrophil Activation law.invention chemistry.chemical_compound Dogs law Internal medicine medicine Cardiopulmonary bypass Animals Sulfones Endothelial dysfunction Cariporide business.industry medicine.disease Blood medicine.anatomical_structure chemistry Coronary occlusion Anesthesia Coronary vessel Heart Arrest Induced Cardiology Female Surgery Endothelium Vascular business Cardiology and Cardiovascular Medicine Reperfusion injury |
| Zdroj: | The Journal of Thoracic and Cardiovascular Surgery. 125(1):155-164 |
| ISSN: | 0022-5223 |
| DOI: | 10.1067/mtc.2003.65 |
| Popis: | Background: Activation of the sodium-hydrogen ion exchange mechanism results in accumulation of intracellular calcium through the sodium-calcium ion antiport mechanism. Administration of a sodium-hydrogen ion exchange inhibitor before or during ischemia attenuates myocardial ischemia and reperfusion injury. However, the cardioprotection exerted by sodium-hydrogen ion exchange inhibitors as adjuncts to cardioplegia without perioperative administration has not been tested in a model of surgical reperfusion of acute coronary occlusion with cardiopulmonary bypass. This study tested the hypothesis that sodium-hydrogen ion exchange inhibitor-supplemented blood cardioplegia would reduce postcardioplegia injury after severe regional ischemia. Methods: In anesthetized open-chest dogs, the left anterior descending coronary artery was occluded for 75 minutes, after which total cardiopulmonary bypass was initiated. After crossclamping, cold (4°C) antegrade blood cardioplegia was delivered every 20 minutes for a total of 60 minutes of cardioplegic arrest. In 8 dogs, the blood cardioplegic solution was unsupplemented (vehicle group), whereas in 8 others the solution was supplemented with the sodium-hydrogen ion exchange inhibitor cariporide (10 μmol/L, cariporide group). Results: In the in vitro studies, the direct effects of cariporide on neutrophil function were determined. Isolated canine neutrophils were stimulated by platelet activating factor. Cariporide attenuated superoxide anion production in a concentration-dependent manner, with no appreciable effect at 10 μmol/L (the concentration used in blood cardioplegia) and a peak effect at 100 μmol/L. In the in vivo cardiopulmonary bypass model, infarct size was significantly (P |
| Databáze: | OpenAIRE |
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