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J Thorac Cardiovasc Surg 1994;108:946-952
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Myocardial buffering capacity and high-energy phosphate utilization during hypothermic circulatory arrest and recovery in the newborn lamb in vivo

Seattle, Wash.

George E. Eyster, VMD

East Lansing, Mich.

From the Department of Pediatrics, University of Washington School of Medicine, Seattle, Wash., and Department of Surgery, Michigan State University College of Veterinary Medicine, East Lansing, Mich.

Received for publication Oct. 27, 1993. Accepted for publication March 16, 1994. Address for reprints: Michael A. Portman, MD, Pediatrics RD-20, University of Washington, Seattle, WA 98195.

Abstract

The purpose of this study was to measure myocardial buffering capacity and adenosine triphosphate utilization rates in the newborn animal in vivo during hypothermic circulatory arrest and recovery. Methods: These studies were performed with ³¹P magnetic resonance spectroscopic techniques, which supplied a 12- to 16-second time resolution, to monitor intracellular pH and phosphocreatine and adenosine triphosphate levels. All experiments were performed with a radiofrequency surface coil on the pericardium with the sheep centered inside a 4.7 T magnet. Newborn sheep (n = 5, aged 16 days ± 2.4 standard error) were supported by cardiopulmonary bypass, cooled to 20° C, and subjected to 20 minutes of circulatory arrest. Results: During early ischemia, phosphocreatine hydrolysis progressed at a linear rate, 1.2 ± 0.05µmol/gm per minute, and was accompanied by intracellular alkalinization. Myocardial buffering capacity calculated frompH/phosphocreatine equals 25 ± 3µeq gm^-1 pH^-1, a value similar to that obtained from perfused heart studies. After the initial 4 minutes in ischemia, the decrease in phosphocreatine hydrolysis was accompanied by intracellular acidification, which is likely due to late induction of anaerobic metabolism. Conclusions: In these studies, early phosphocreatine hydrolysis rate is nearly equivalent to adenosine triphosphate utilization rate. During the early period of ischemia phosphocreatine hydrolysis serves a buffering function and is associated with intracellular alkalinization. These techniques and measurements can be used to compare effects of myocardial preservation techniques on intracellular pH and adenosine triphosphate kinetics. (J THORAC CARDIOVASC SURG 1994;108:946-52)

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