Non Steroidal and Non Barbiturate Treatment of Secondary Brain Damage

  • Petter A. Steen
  • S. E. Gisvold
  • L. A. Newberg
  • W. L. Lanier
  • B. W. Scheithauer
  • J. D. Michenfelder
Part of the NATO ASI Series book series (NSSA, volume 115)


Drug treatment in cerebral hypoxia is after decades of research still controversial, and no treatment appears to be established at the moment. Not even the mechanisms causing the primary or possible secondary damage are established (Siesjö, 1981), only that they are obviously linked to a disturbance in the oxygen demand/oxygen supply ratio. Many hypotheses have been recently advanced involving increased intracellular concentrations of free calcium as responsible for large parts also of the secondary brain damage (Raichle, 1982; Siesjö, 1981; White et al., 1983a). In Michenfelders’s laboratory at the Mayo Clinic we have especially studied complete cerebral ischemia. Secondary brain damage in the post-ischemic period due to a disturbed calcium homeostasis could include decreased CBF due to vasospasm (Somlyo and Somlyo, 1968; Van Neuten and Vanhoutte, 1980; Vanhoutte, 1981), reduced blood cell deformability (DeCree, et al. 1979), and platelet aggregation (Vanhoutte and Van Neuten, 1980). These factors could either be due to direct Ca++ effects or indirectly to a calcium stimulated breakdown of arachidonic acid to products such as prostaglandins, leukotrienes or thromboxanes (Raichle, 1982; Siesjö, 1981).


Cereb Blood Flow Calcium Entry Blocker Calcium Blocker Secondary Brain Damage Cerebral Cortical Blood Flow 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • Petter A. Steen
    • 1
  • S. E. Gisvold
    • 1
  • L. A. Newberg
    • 1
  • W. L. Lanier
    • 1
  • B. W. Scheithauer
    • 1
  • J. D. Michenfelder
    • 1
  1. 1.Department of AnesthesiologyUniversity of Oslo, Ulleval HospitalOslo 1Norway

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