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Ann Thorac Surg 1980;30:472-481
© 1980 The Society of Thoracic Surgeons
From the Cardiovascular Laboratories, Banting Institute, University of Toronto, and the Department of Anesthesia, Hospital for Sick Children, Toronto, Ont, Canada
* Address reprint requests to Dr. MacGregor, Director, Cardiovascular Laboratories, Room 68, Banting Institute, 100 College Street, Toronto, Ont, Canada M5G 1L5
Using an intramyocardial pH needle probe (21 gauge) to monitor myocardial metabolism during ischemia, we determined the effect of potassium cardioplegia at both moderate and deep hypothermia. Five groups of 5 dogs each were placed on cardiopulmonary bypass and the pH probe was inserted approximately 10 mm into the left ventricular free wall. Cardiac ischemia was achieved by cross-clamping the ascending aorta at 37°C (Group 1), 27°C (Group 2), or 17°C (Group 3). In the remaining two groups, aortic cross-clamping was followed by the infusion of 600 to 800 ml of potassium cardioplegic solution adjusted to cardiac temperatures of 27°C (Group 4) or 17°C (Group 5). In each group, myocardial temperature was maintained constant, electrical and mechanical activity observed, and pH recorded until a plateau was reached or for 3 hours.
Our results show a progressive and significant decrease in the metabolic rate with reduction in temperature over the 37° to 17°C range. By abolishing contractile activity, potassium cardioplegia markedly reduces the rate of hydrogen ion accumulation at 27 °C, but at 17 °C the additive effect of cardioplegia is much less pronounced. These observations support the principle of reducing contractile activity to a minimum during elective arrest of the heart but indicate that potassium cardioplegia does little to further reduce the rate of anaerobic metabolism, as shown by the measurement of intramyocardial pH, under conditions of deep hypothermia.
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