title: Does the redox state of cytochrome aa3 reflect brain energy level during hypoxia? Simultaneous measurements by near infrared spectrophotometry and 31P nuclear magnetic resonance spectroscopy.
abstract: We studied cerebral oxygen metabolism during hypoxia to demonstrate whether the redox state of cytochrome aa3 (cyt.aa3), as measured by near infrared spectrophotometry (NIRS), reflects brain energy level. Rats (n = 6) subjected to hypoxia were simultaneously monitored by NIRS and 31P nuclear magnetic resonance spectroscopy (NMRS). Brain function was evaluated using the electroencephalogram (EEG). After a reduction of the fraction of inspired oxygen FIO2 from 0.21 to 0.15, we observed a significant increase in reduced cyt.aa3 (from 16.5% +/- 2.1% to 41.2% +/- 2.8%; P < 0.01), without significant changes in phosphocreatine (PCr) and beta-adenosine triphosphate (beta-ATP) levels. The PCr decreased significantly at a FIO2 of 0.10 (53.8% +/- 6.4% as compared with 97.7% +/- 10.9% at a FIO2 of 0.21; P < 0.05), and reached a minimum at a FIO2 of 0.04. beta-ATP did not change significantly at a FIO2 of 0.10 or 0.08. With a FIO2 of less than 0.08, cyt.aa3 was almost totally reduced. EEG activity slowed at a FIO2 of 0.08 and became isoelectric at 0.04. Significant correlations were found between the levels of cyt.aa3 and PCr (P < 0.001, r = 0.83) as well as between cyt.aa3 and beta-ATP (P < 0.001, r = 0.73) by using the overall values at FIO2 levels from 0 to 1.0. However, no significant correlations were observed among these variables when the FIO2 was less than 0.10. These findings suggest that the increase in reduced cyt.aa3 reflects brain energy depletion; however, the redox state of cyt.aa3 will not indicate brain energy depletion during extreme hypoxia because cyt.aa3 is reduced totally during hypoxia insufficient to deplete intracellular ATP.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Kagoshima University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Oda
authors.forename: M A
authors.initials: MA
authors.lastname: Hossain
authors.forename: N
authors.initials: N
authors.lastname: Yoshimura
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004569:Electroencephalography; D003576:Electron Transport Complex IV / Q000378:metabolism*; D004734:Energy Metabolism; D006454:Hemoglobins / Q000032:analysis; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000503:physiopathology; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D010084:Oxidation-Reduction; D010108:Oxyhemoglobins / Q000032:analysis; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013055:Spectrophotometry, Infrared
chemical_list: D006454:Hemoglobins; D010108:Oxyhemoglobins; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; C100003:deoxyhemoglobin; D003576:Electron Transport Complex IV