Hyperglycemia During Hypothermic Cardiopulmonary Bypass Does Not Alter Postbypass Vascular Endothelial Responses in Dogs

Background: Hyperglycemia during hypothermic cardiopulmonary bypass (CPB) may alter intrinsic vasomotion by reducing endothelial-dependent vasorelaxation. Using a canine model of hypothermic CPB, this study tested whether hyperglycemia altered the vasodilator response to acetylcholine (ACh) and the vasoconstrictor response to phenylephrine (Phe). Methods: In 20 anesthetized dogs, the left femoral arteries were excised and placed in gassed (95% O 2 -5% CO 2 ) cold Krebs's solution. The animals were randomized into two groups undergoing 120 minutes of 28°C CPB using membrane oxygenators. A hyperglycemic group ( n = 10) received a continuous infusion of 50% dextrose to maintain blood glucose level greater than 500 mg/dL; a normoglycemic group ( n = 10) received 0.9% saline. After rewarming and discontinuing CPB, the right femoral arteries were excised. Vessel rings were placed in a suffusion bath, and changes in isometric tension were measured. Dose-response relationships (ACh: 10 −9 to 10 −6 M; Phe: 3 × 10 −8 to 10 −4M and -log ED 50 sensitivity to ACh and Phe before and after CPB were compared. Results: Serum glucose during hypothermic CPB was significantly greater in glucose-treated dogs (525 ± 9 mg/dL) than controls (109 ± 5 mg/dL; p 50 values for ACh changed from 7.7 ± 0.1 to 7.5 ± 0.2 ( p p Conclusions: The reduction in ACh-mediated vasorelaxation after CPB did not differ between hyperglycemic and normoglycemic animals, indicating that hyperglycemia does not contribute to impaired vasorelaxation after CPB. Because Phe-induced vasoconstriction was unaffected, hyperglycemia during hypothermic CPB does not appear to increase the potential for postbypass vasospasm.