HYPERGLYCEMIA DURING HYPOTHERMIC CANINE CARDIOPULMONARY BYPASS INCREASES CEREBRAL LACTATE

Background: Hyperglycemia frequently occurs during cardiopulmonary byp ass (CPB), although its direct effects on cerebral perfusion and metab olism are not known. Using a canine model of hypothermic CPB, we teste d whether hyperglycemia alters cerebral blood flow and metabolism and cerebral energy charge. Methods: Twenty anesthetized dogs were randomi zed into hyperglycemic (n = 10) and normoglycemic (n = 10) groups. The hyperglycemic group received an infusion of D50W, and the normoglycem ic animals received an equal volume of 0.9% NaCl. Both groups underwen t 120 min of hypothermic (28 degrees C) CPB using membrane oxygenators , followed by rewarming and termination of CPB, Cerebral blood flow (r adioactive microspheres) and the cerebral metabolic rate for oxygen we re measured intermittently during the experiment and brain tissue meta bolites were obtained after bypass. Results: Before CPB, the glucose-t reated animals had higher serum glucose levels (534+/-12 mg/dL; mean /- SE) than controls (103+/-4 mg/dL; P<0.05), and this difference was maintained throughout the study. Cerebral blood flow and metabolism di d not differ between groups at any time during the experiment, Sagitta l sinus pressure was comparable between groups throughout CPB. Tissue high-energy phosphates and water contents were similar after CPB, alth ough cerebral lactate levels were greater in hyperglycemic (37.2+/-5.7 mu mol/g) than normoglycemic animals (19.7+/-3.7 mu mol/g; P<0.05). A fter CPB, pH values of cerebrospinal fluid for normoglycemic (7.33+/-0 .01) and hyperglycemic (7.34+/-0.01) groups were similar. Conclusions: Hyperglycemia during CPB significantly increases cerebral lactate lev els without adversely affecting cerebral blood flow and metabolism, ce rebrospinal fluid pH, or cerebral energy charge.