Disturbances of Extracellular pK, pNa and pH During No-Flow Anoxia

  • J. Höper
  • M. Kessler
  • S. Ji
  • H. Acker
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 92)


It has been known for many years that immediately after the onset of ischemia (no-flow anoxia) a fast depletion of cellular energy-rich phosphates occurs (Thorn et al., 1957; Brettschneider 1964, Brosnan et al. 1970, Chance et al. 1965, Schmahl et al. 1966, see Cohen 1973). In contrast to no-flow anoxia, a norm-flow anoxia (anoxic anoxia) is tolerated over a longer period of time (Höper et al. 1973, Kessler et al. 1974, 1976 a, b). Already in 1953 Opitz considered that during no-flow anoxia the acidosis caused by accumulation of lactic acid may be responsible for the irreversible cellular damage of the brain, but the cellular mechanisms which cause the cellular alterations have not yet been explained completely.


Lactic Acid Anaerobic Glycolysis Tissue Oxygen Tension Extracellular Sodium Lactate Content 
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Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • J. Höper
    • 1
  • M. Kessler
    • 1
  • S. Ji
    • 1
  • H. Acker
    • 1
  1. 1.Max-Planck-Institut für SystemphysiologieRheinlanddamm 201Germany

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