Reduction of cytochrome-c-oxidase copper precedes failing cerebral
oxygen utilization in fluorocarbon perfused cats.
Stingele, R., B. Wagner, M. V. Kameneva, M. A. Williams, D. A. Wilson,
N. V. Thakor, R. J. Traystman, D. F. Hanley.
Departments of Neurology, Anesthesiology/Critical Care Medicine,
and Biomedical Engineering, The Johns Hopkins Medical Institutions,
Baltimore, MD 21287 and Department of Surgery, University of
Pittsburgh, Pittsburgh, PA 15219
APStracts 3:0029H, 1996.
We determined the relationship of the low potential copper (CuA)redox
state of cytochrome-c-oxidase to the brain tissue partial pressure of
oxygen (PtO2) and global cerebral oxygen consumption (CMRO2) in vivo.
The redox state of cytochrome-c-oxidase copper was monitored in
perfluorocarbon exchanged cats under normoxic and graded hypoxic
conditions using near infrared spectroscopy (NIRS). Continuous
spectra ranging from 730 nm to 960 nm were acquired and the change in
copper redox state was assessed by the absorption changes at 830 nm.
PtO2 was measured with oxygen sensitive electrodes implanted into
cortex and CMRO2 was determined by sampling arterial and superior
sagittal sinus perfusate and by measuring blood flow with
radiolabelled microspheres. As brain PtO2 decreased with hypoxia, the
low potential copper-site (CuA) of cytochrome-c-oxidase became
progressively reduced, whereas the cerebral metabolic rate of oxygen
(CMRO2) was unchanged during the initial stages of hypoxia. Only with
severe hypoxia, did CMRO2 and the amplitude of somatosensory evoked
potentials decrease. We conclude that the CuA-site of cytochrome-c
-oxidase is involved in a regulatory adjustment that helps to maintain
CMRO2 constant.
Received 8 August 1995; accepted in final form 2 January 1996.
APS Manuscript Number H743-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 January 96