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Ann Thorac Surg 1976;22:557-571
© 1976 The Society of Thoracic Surgeons
From the Departments of Surgery, New York University Medical Center, New York, NY, and The Abraham Lincoln School of Medicine, University of Illinois at the Medical Center, and The Veterans Administration West Side Hospital, Chicago, IL
* Address reprint requests to Dr. Engelman, The Abraham Lincoln School of Medicine, 840 S Wood St, Chicago, IL 60680
The relative efficacy of potassium-induced ischemic arrest using buffered, isosmotic potassium (25 mEq/liter) was compared with hypothermic arrest in an experimental protocol employing an intact canine heart preparation. Myocardial function (LVSW, dp/dt max), serum creatine phosphokinase levels, myocardial perfusion, and light and electron microscopical examination of the heart were assessed in five groups of 5 dogs each. There was one control group (90 minutes of bypass, no anoxia) and four experimental groups, each subjected to 1 hour of ischemic arrest and 30 minutes of reperfusion, comparing normothermic ischemic arrest (NIA), hypothermic ischemic arrest (myocardial temperature < 25°GC) (HIA), normothermic potassium arrest (NKA), and hypothermic potassium arrest (HKA).
Myocardial function decreased significantly following NIA and NKA but remained essentially equal in the control, HIA, and HKA groups. Serum creatine phosphokinase analysis documented a significant increase in each group of animals: 2,250 mU after NIA, 1,778 mU after NKA, 1,338 mU after HIA, 1,220 mU after HKA, and 838 mU after control bypass. Left ventricular myocardial perfusion was unmeasurably low after NIA, reduced to 111 ml/100 gm of tissue/min after NKA, and increased to 165 to 188 ml/100 gm/min in the control, HIA, and HKA groups. Electron microscopical studies showed a range of myocardial changes, from probably irreversible damage after NIA to similar but less diffuse changes after NKA, and to potentially reversible changes after HKA and HIA, with the least alteration from control after HIA.
The results indicate that potassium arrest alone is not as effective as hypothermia in preventing ischemic injury, and the combination of hypothermia with a single 150 cc administration of potassium (25 mEq/liter) does not appear to provide significant additional protection.
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