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J Thorac Cardiovasc Surg 2001;122:753-758
© 2001 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
From the Departments of Physiology and Surgery, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
Supported by The Heart & Stroke Foundation of Ontario (grant T2454). Karim S. Bandali is supported by a fellowship from The Natural Sciences and Engineering Research Council of Canada (NSERC).
Received for publication Nov 30, 2000. Revisions requested Jan 22, 2001; revisions received March 3, 2001. Accepted for publication March 9, 2001. Address for reprints: C. Wittnich, MSc, DVM, University of Toronto, Medical Sciences Building, Room 7256, 1 King&'s College Circle, Toronto, Ontario M5S 1A8, Canada (E-mail: c.wittnich{at}utoronto.ca).
Objective: We sought to identify whether elevated PaO2 itself can directly cause hyperglycemia in newborns and to document any additional effects of cardiopulmonary bypass on this response.
Methods: Piglets were exposed to either normoxia (88 ± 6 mm Hg) or hyperoxia (470 ± 28 mm Hg) in the following studies. Anesthetized 3-day-old neonatal pigs were either ventilated for 2 hours of normoxia (n = 5) or hyperoxia (n = 5) or placed on normothermic, normoxic cardiopulmonary bypass (n = 6) and then randomly assigned to either undergo a 2-hour normoxic period or a 1-hour hyperoxic episode, followed by a return to normoxia for an additional hour. Blood glucose levels were measured in all animals.
Results: No significant changes were observed in blood glucose levels in neonatal pigs that underwent 2 hours of normoxic ventilation (5.0 ± 0.6 mmol/L) or cardiopulmonary bypass (6.6 ± 1.6 mmol/L). However, the ventilatory model showed a significant and sustained (P < .001) hyperglycemic response after both 1 hour (8.6 ± 1.0 mmol/L) and 2 hours (9.8 ± 1.6 mmol/L) of hyperoxia. In the cardiopulmonary bypass model, exposure to 1 hour of hyperoxia elicited a significant (P < .05) hyperglycemic response (10.3 ± 1.2 mmol/L), followed by a return to normal blood glucose levels (6.6 ± 1.6 mmol/L) with a return to normoxia. This hyperoxia-mediated hyperglycemic response was confirmed when data examined from children undergoing cardiopulmonary bypass for primary repair of their congenital defects also identified a significant positive correlation (r = 0.72, P = .02) between oxygen levels and blood glucose levels measured before and at the end of cardiopulmonary bypass.
Conclusions: Hyperoxia triggers a hyperglycemic response in both ventilatory and bypass models. Cardiopulmonary bypass does not exacerbate this response, as shown by the similar levels of hyperglycemia sustained for the duration of the hyperoxic exposure in both experimental models. Therefore, not only may hyperoxia play a crucial role in the hyperglycemic response seen during neonatal cardiopulmonary bypass, but its effect on glucose homeostasis should be considered whenever children are exposed to hyperoxia.
This article has been cited by other articles:
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  K. S. Bandali, M. P. Belanger, and C. Wittnich Hyperoxia causes oxygen free radical-mediated membrane injury and alters myocardial function and hemodynamics in the newborn Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H553 - H559. [Abstract] [Full Text] [PDF]
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 K. S. Bandali, M. P. Belanger, and C. Wittnich Does hyperoxia affect glucose regulation and transport in the newborn? J. Thorac. Cardiovasc. Surg., December 1, 2003; 126(6): 1730 - 1735. [Abstract] [Full Text] [PDF]
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