Hyperglycemia during hypothermic cardiopulmonary bypass does not alter postbypass vascular endothelial responses in...

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).

In 20 anesthetized dogs, the left femoral arteries were excised and placed in gassed (95% O2-5% CO2) cold Krebs's solution. The animals were randomized into two groups undergoing 120 minutes of 28 degrees 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 x 10(-8) to 10(-4)M) and -log ED50 sensitivity to ACh and Phe before and after CPB were compared.

Serum glucose during hypothermic CPB was significantly greater in glucose-treated dogs (525 +/- 9 mg/dL) than controls (109 +/- 5 mg/dL; p < 0.05). After CPB, -log ED50 values for ACh changed from 7.7 +/- 0.1 to 7.5 +/- 0.2 (p < 0.05) in normoglycemic dogs and from 7.8 +/- 0.1 to 7.6 +/- 0.1 (p < 0.05) in hyperglycemic animals, indicating similar and significant rightward shifts of the dose-response relationship to ACh after CPB in both groups. Neither hyperglycemia nor CPB altered the vasoconstrictor response to Phe.

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.