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Ann Thorac Surg 1983;35:605-614
© 1983 The Society of Thoracic Surgeons
From the Departments of Surgery and Medicine, Cardiothoracic Section, Veterans Administration Medical Center, and State University of New York at Buffalo School of Medicine, Buffalo, NY
Accepted for publication August 12, 1982.
* Address reprint requests to Dr. Balderman, Assistant Professor of Surgery, Veterans Administration Medical Center, 3495 Bailey Ave, Buffalo, NY 14215
To determine the myocardial temperature that provides maximal preservation of the heart during global ischemic arrest, five groups of dogs were studied (6 per group). In all animals, the aorta was cross-clamped for 120 minutes. Serial biopsies were done for determination of adenosine triphosphate and creatine phosphate, and study by electron microscopy. Starling curves were derived prior to cardiopulmonary bypass and 60 minutes after bypass. Mitochondrial changes were graded on a scale of 0 to 4. In the control group (Group 1), the aorta was clamped when the rectal temperature reached 25°C (myocardial temperature, 18° to 22°C). In Groups 2, 3, 4, and 5, myocardial temperature was maintained at 6°C, 10°C, 14°C, and 18°C (all ± 2°C), respectively, by the use of systemic and topical hypothermia and repeated injections of cold cardioplegia solution into the aortic root. All groups showed a depression of left ventricular stroke work index, particularly Group 1 (no survivors), Group 2, and Group 3. The high-energy phosphate stores were well preserved in all groups except Group 1. The mitochondrial ultrastructure showed significant changes in all groups, especially Groups 1 and 5.
These data indicate that satisfactory preservation of mitochondrial ultrastructure and high-energy phosphates was achieved at myocardial temperatures lower than 18°C. Extreme hypothermia (Groups 2 and 3) was associated with significant reduction in ventricular function under the experimental conditions employed.
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