Disturbances of Cellular Membranes and Membrane-Bound Enzymes in Cryogenic Brain Edema

  • Francois Cohadon
  • N. Averet
  • M. Rigoulet
Part of the NATO ASI Series book series (NSSA, volume 115)


The hypothesis of cellular membrane dysfunction playing a key role in the pathophysiology of acute brain damage is not new. As early as 1966 Ishii (1) using an epidural balloon injury model has shown a loss of essential membrane phospholipids, namely of lecithin and gangliosides, and an impairment of ATPase function in brain tissue. Both phenomena were roughly proportional to the deterioration of the animals condition. In an attempt to explain the beneficial effect of corticosteroids, Demopoulos et al. (2) proposed an attack of free radicals on phospholipids as a mechanism of membrane damage. The fact that antioxidants were capable to diminish cold injury edema significantly (3) was a supporting argument. The “membrane theory” of brain damage has been extensively discussed since then for a number of acute brain conditions (cf.: 4).


ATPase Activity Brain Edema Regional Cerebral Blood Flow Vasogenic Edema Rabbit Brain 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • Francois Cohadon
    • 1
  • N. Averet
    • 1
  • M. Rigoulet
    • 1
  1. 1.Laboratoire de Neurochirurgie Experimentale et NeurobiologieUniversite de Bordeaux II, Service de Neurochirurgie ABordeauxFrance

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