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Canadian Journal of Anesthesia 50:1061-1068 (2003)
© Canadian Anesthesiologists' Society, 2003

Neuroanesthesia and Intensive Care

Hypercapnia increases cerebral tissue oxygen tension in anesthetized rats

[L’hypercapnie augmente la tension en oxygène du tissu cérébral chez des rats anesthésiés]

Gregory M.T. Hare, MD PhD*, Brian P. Kavanagh, MB{dagger}, C. David Mazer, MD*, Kathryn M. Hum*, Steve Y. Kim*, Carla Coackley*, Aiala Barr, PhD{ddagger} and Andrew J. Baker, MD*

* From the Department of Anaesthesia,
{ddagger} the Department of Public Health, St. Michael’s Hospital;
{dagger} and the Department of Critical Care Medicine, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.

Address correspondence to: Dr. Gregory M.T. Hare, Department of Anaesthesia, University of Toronto, St. Michael’s Hospital, 30 Bond Street, Toronto, Ontario M5B 1W8, Canada. Phone: 416-864-5259; Fax: 416-864-6014; E-mail hareg{at}smh.toronto.on.ca

Purpose: To test the hypotheses that deliberate elevation of PaCO2 increases cerebral tissue oxygen tension (PBrO2) by augmenting PaO2 and regional cerebral blood flow (rCBF).

Methods: Anesthetized rats were exposed to increasing levels of inspired oxygen (O2) or carbon dioxide (CO2; 5%, 10% and 15%, n = 6). Mean arterial blood pressure (MAP), PBrO2 and rCBF were measured continuously. Blood gas analysis and hemoglobin concentrations were determined for each change in inspired gas concentration. Data are presented as mean ± standard deviation with P < 0.05 taken to be significant.

Results: The PBrO2 increased in proportion to arterial oxygenation (PaO2) when the percentage of inspired O2 was increased. Proportional increases in PaCO2 (48.7 ± 4.9, 72.3 ± 6.0 and 95.3 ± 15.4 mmHg), PaO2 (172.2 ± 33.1, 191.7 ± 42.5 and 216.0 ± 41.8 mmHg), and PBrO2 (29.1 ± 9.2, 49.4 ± 19.5 and 60.5 ± 23.0 mmHg) were observed when inspired CO2 concentrations were increased from 0% to 5%, 10% and 15%, respectively, while arterial pH decreased (P < 0.05 for each). Exposure to CO2 increased rCBF from 1.04 ± 0.67 to a peak value of 1.49 ± 0.45 (P < 0.05). Following removal of exogenous CO2, arterial blood gas values returned to baseline while rCBF and PBrO2 remained elevated for over 30 min. The hypercapnia induced increase in PBrO2 was threefold higher than that resulting from a comparable increase in PaO2 achieved by increasing the inspired O2 concentration (34.9 ± 14.5 vs 11.4 ± 5.0 mmHg, P < 0.05).

Conclusion: These data support the hypothesis that the combined effect of increased CBF, PaO2 and reduced pH collectively contribute to augmenting cerebral PBrO2 during hypercapnia.




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