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Ann Thorac Surg 1985;39:312-317
© 1985 The Society of Thoracic Surgeons
From the Departments of Thoracic Surgery and Cardiology, University of Leiden, Leiden, The Netherlands
Accepted for publication June 7, 1984.
* Address reprint requests to Dr. Schipperheyn, Department of Cardiology, Academic Hospital, Rijnsburgerweg 10, 2333 AA Leiden, The Netherlands
Isolated pumping rat hearts, perfused with reconstituted blood, were studied to compare the effects of 30 minutes of ischemic arrest following calcium-free or normal, calcium-containing cold cardioplegia on recovery of mechanical function, lactate production, myocardial adenosine triphosphate concentration, and release of creatine kinase (CK). As in clinical situations, the volume of the infusate was only three to four times the intracavitary blood volume.
Hearts arrested with calcium-free solution showed incomplete recovery of mechanical function, whereas hearts arrested with calcium-containing solution recovered completely. After calcium-free arrest, stroke volume recovered to 76 ± 29% (standard deviation [SD]) of its prearrest value. Enzyme release (CK) was significantly higher after calcium-free cardioplegia (7.7 ± 4.6 units [SD]) than after cardioplegia with normal calcium (2.1 ± 1.6 units [SD]). Since the addition of only 0.025 mmol calcium ions to a liter of calcium-free solution completely prevented its negative effect, it was concluded that calcium-free cardioplegia may cause limited but pronounced damage to myocardial cells, presumably because it removes calcium from the cellular membranes—the so-called calcium paradox. Probably due to residual calcium in blood and extracellular fluid, the damage is not so extensive after calcium-free cardioplegia as to be noticeable in clinical surgical situations. Residual calcium in the heart does not exclude the possibility, however, that a calcium paradox occurs in small scattered areas of the heart.
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