Advertisement

Responses of Electrical Activity and Redox State of Cytochrome Oxidase to Oxygen Insufficiency in Perfused Rat Brain In Situ

  • Y. Nomura
  • A. Matsunaga
  • M. Tamura
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 388)

Abstract

During the transition from normoxia to hypoxia in brain tissue, the energy related metabolites remain unchanged until the cerebral oxygen consumption decreases. For example, ATP levels are kept normal at arterial oxygen tensions higher than around 25 mmHg. Below this, ATP begins to decrease together with the increases of ADP and AMP, where oxygen consumption decreases. The electrical activity is also attenuated. The activation of glycolytic flux prevents, in part, the decline of ATP (Sylvia and Piantadosi, 1988, Erecinska and Silver, 1989). In addition, it has been reported that neuronal activity is suppressed prior to decreases in ATP. Thus, the energy failure is not solely responsible for suppression of brain function in hypoxic conditions. Previously, we have calibrated the oxygen dependence of the redox centers of cytochrome oxidase, heme aa3 and copper, in isolated mitochondria (Hoshi et al., 1993). The redox state of heme aa3 depends on both the energy state and the respiratory rate, whereas the redox state of copper is independent of both the energy state and the respiratory rate. Thus, simultaneous measurements of these chromophores in cytochrome oxidase can give both oxygen concentration and energy state at mitochondria. On the basis of the in vitro data of isolated mitochondria, we measured the redox state of cytochrome oxidase and the electrical activity in perfused rat brain in situ. The relationship between functional failure and oxygen insufficiency became much clearer from the present study, which is presented here.

Keywords

Redox State Hypoxic Condition Cytochrome Oxidase Oxygen Insufficiency Perfuse Brain 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Erecinska, M., and Silver, I. A., 1989, ATP and brain function, J. Cereb. Blood Flow Metab. 9: 2–19.PubMedCrossRefGoogle Scholar
  2. Harvey, S. A. K., Trankina, M. L., Olson, M. S., and Clark, J. B., 1991, Fluorocarbon perfusion of the isolated rat brain: measurement of tissue spaces, EEG and oxygen uptake, Biochim. Biophys. Acta. 1073: 486–492.PubMedGoogle Scholar
  3. Hoshi, Y., Hazeki, O., and Tamura, M., 1993, Oxygen dependence of redox state of copper in cytochrome oxidase in vitro, J. Appi. Physiol. 74: 1622–1627.Google Scholar
  4. Inagaki, M., and Tamura, M., 1993, Preparation and optical characteristics of hemoglobin-free isolated perfused rat head in situ, J. Biochem. 113: 650–657.PubMedGoogle Scholar
  5. Sylvia, A. L., and Piantadosi, C. A., 1988, 02 dependence of in vivo brain cytochrome redox responses and energy metabolism in bloodless rats, J. Cereb. Blood Flow Metab. 8: 163–172.PubMedCrossRefGoogle Scholar
  6. Tamura, M., Hazeki, O., Nioka, S., Chance, B. and Smith, D. S., 1988, The simultaneous measurements of tissue oxygen concentration and energy state by near-infrared and nuclear magnetic resonance spectroscopy, Adv. Exp. Med. Biol. 222: 359–363.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1996

Authors and Affiliations

  • Y. Nomura
    • 1
  • A. Matsunaga
    • 1
  • M. Tamura
    • 1
  1. 1.Biophysics group, Research Institute for Electronic ScienceHokkaido UniversitySapporoJapan

Personalised recommendations