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Ann Thorac Surg 1992;54:1126-1130
© 1992 The Society of Thoracic Surgeons

Articles

Hyperglycemia increases cerebral intracellular acidosis during circulatory arrest

Richard V. Anderson, MDa,b, Michael G. Siegman, MDa,b, Robert S. Balaban, PhDa,b, Toni L. Ceckler, PhDa,b, Julie A. Swain, MD*,a,b

a Surgery Branch and Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
b Department of Surgery, University of Nevada School of Medicine, Las Vegas, Nevada, USA

Accepted for publication March 23, 1992.

* Address reprint requests to Dr Swain, Division of Cardiovascular Surgery, University of Nevada School of Medicine, 2040 W Charleston Blvd, Suite 601, Las Vegas, NV 89102.

Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess cerebral high-energy phosphate metabolism and intracellular pH in normoglycemic and hyperglycemic sheep during hypothermic circulatory arrest. Two groups of sheep (n = 8 per group) were placed in a 4.7-T magnet and cooled to 15 °C using cardiopulmonary bypass. Spectra were acquired before and during circulatory arrest and during reperfusion and rewarming. Intracellular pH and adenosine triphosphate levels decreased during circulatory arrest. Compared with the normoglycemic animals, the hyperglycemic group was significantly more acidotic with the greatest difference observed during the first 20 minutes of reperfusion (6.40 ± 0.08 versus 6.08 ± 0.06; p < 0.001). Intracellular pH returned to baseline after 30 minutes of reperfusion in the normoglycemic group but did not reach baseline until 1 hour of reperfusion in the hyperglycemic animals. Adenosine triphosphate levels were significantly higher in the hyperglycemic group during circulatory arrest. Repletion of adenosine triphosphate during reperfusion was similar for both groups. These results support the hypothesis that hyperglycemia during cerebral ischemia drives anaerobic glycolysis and thus leads to increased lactate production and a decrease in the intracellular acidosis normally associated with ischemia.




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