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
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