HYPERGLYCEMIA DURING HYPOTHERMIC CARDIOPULMONARY BYPASS DOES NOT ALTER POSTBYPASS VASCULAR ENDOTHELIAL RESPONSES IN DOGS

Citation
C. Odwyer et al., HYPERGLYCEMIA DURING HYPOTHERMIC CARDIOPULMONARY BYPASS DOES NOT ALTER POSTBYPASS VASCULAR ENDOTHELIAL RESPONSES IN DOGS, Journal of cardiothoracic and vascular anesthesia, 10(5), 1996, pp. 614-618
Citations number
20
Categorie Soggetti
Anesthesiology,"Peripheal Vascular Diseas","Cardiac & Cardiovascular System
ISSN journal
10530770
Volume
10
Issue
5
Year of publication
1996
Pages
614 - 618
Database
ISI
SICI code
1053-0770(1996)10:5<614:HDHCBD>2.0.ZU;2-9
Abstract
Background:; Hyperglycemia during hypothermic cardiopulmonary bypass ( CPB) may alter intrinsic vasomotion by reducing endothelial-dependent vasorelaxation. Using a canine model of hypothermic Cps, this study te sted whether hyperglycemia altered the vasodilator response to acetylc holine (ACh) and the vasoconstrictor response to phenylephrine (Phe). Methods: In 20 anesthetized dogs, the left femoral arteries were excis ed and placed in gassed (95% O-2-5% CO2) cold Krebs's solution. The an imals were randomized into two groups undergoing 120 minutes of 28 deg rees C CPB using membrane oxygenators. A hyperglycemic group (n = 10) received a continuous infusion of 50% dextrose to maintain blood gluco se level greater than 500 mg/dL; a normoglycemic group (n = 10) receiv ed 0.9% saline. After rewarming and discontinuing Cps, the right femor al arteries were excised. Vessel rings were placed in a suffusion bath , and changes in isometric tension were measured. Dose-response relati onships (ACh: 10(-9) to 10(-6) M; Phe: 3 x 10(-8) to 10(-4) M) and -lo g ED(50) sensitivity to ACh and Phe before and after CPB were compared . Results: Serum glucose during hypothermic CPB was significantly grea ter in glucose-treated dogs (525 +/- 9 mg/dL) than controls (109 +/- 5 mg/dL; p < 0.05). After CPB, -log ED(50) 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, indicat ing similar and significant rightward shifts of the dose-response rela tionship to ACh after CPB in both groups. Neither hyperglycemia nor CP B altered the vasoconstrictor response to Phe. Conclusions: The reduct ion in ACh mediated vasorelaxation after CPB did not differ between hy perglycemic and normoglycemic animals, indicating that hyperglycemia d oes not contribute to impaired vasorelaxation after CPB. Because Phe-i nduced vasoconstriction was unaffected, hyperglycemia during hypotherm ic CPB does not appear to increase the potential for postbypass vasosp asm. Copyright a 1996 by W.B. Saunders Company