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% 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.
Results: 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.
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.
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http://dx.doi.org/10.1016/s1053-0770(96)80139-x | DOI Listing |
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