Mechanisms of Cerebral Hypoxia and Stroke

1. Front Matter

   Pages i-xii

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2. Adaptation in Diving Vertebrates

   1. Inborn Resistance to Hypoxia and the O2-Dependence of Metabolism

      • P. W. Hochachka

      Pages 1-7

   2. Brain Vulnerability and Survival during Anoxia: Protective Strategies of Hypoxia-Resistant Vertebrates

      • Myron Rosenthal, Zi-Cai Feng, Thomas J. Sick

      Pages 9-21

3. General Pathology

   1. Early and Late Neuronal Damage Following Cerebral Ischemia

      • Takaaki Kirino, Akira Tamura, Keiji Sano

      Pages 23-34

   2. Selective Neuronal Cell Death after Transient Forebrain Ischemia in the Mongolian Gerbil

      • Barbara J. Crain, J. Victor Nadler

      Pages 35-47

   3. Possible Implications of Ischemic Damage to Dentate Hilar Somatostatin Neurons in the Rat

      • Flemming Fryd Johansen, Jens Zimmer, Nils Henrik Diemer

      Pages 49-49

   4. Regulation of Glutamate Receptors in Hippocampus after Cerebral Ischemia

      • Eva Valente, Flemming Fryd Johansen, Nils Henrik Diemer

      Pages 51-51

   5. Role of Edema in Pathophysiology of Ischemic Injury

      • Igor Klatzo

      Pages 53-56

   6. Acidosis-Related Brain Damage: Immediate and Delayed Events

      • Maj-Lis Smith, Bo K. Siesjö

      Pages 57-71

   7. Pathology of Ischaemic Brain Damage — Implications for Therapy

      • W. Meier-Ruge, D. Theodore, J. Abraham

      Pages 73-81

   8. Ischemic Damage of Rat Hippocampus and Basal Ganglia: Light Microscopical and Biochemical Changes

      • Rainald Schmidt-Kastner, Wulf Paschen, Janus Szymas, Konstantin-Alexander Hossmann

      Pages 83-90

4. Pathophysiology

   1. Physiological Aspects of Brain Ischaemia in the Experimental Primate and Man

      • Lindsay Symon

      Pages 91-107

   2. The Dependency of Cerebral Ischemic Damage on Duration and Severity of Ischemia: Studies of Single Cell Activity and Multimodality Evoked Responses

      • R. Graf, W.-D. Heiss, K. Kataoka, G. Rosner, A. Wakayama

      Pages 109-117

   3. Microcirculation and Metabolism in Reversible and Irreversible Cerebral Ischemia

      • Eors Dora, Arisztid G. B. Kovach, Joel H. Greenberg, Kortaro Tanaka, Nicholas H. Gonatas, Martin Reivich

      Pages 119-133

   4. Cerebral Blood flow and Its Responsiveness to CO2 after Traumatic and Ischemic Brain Injuries

      • Y. E. Moskalenko, G. B. Weinstein, V. E. Parfenov, M. Bodó, B. V. Gaidar

      Pages 135-136

   5. The Correlation between Electrophysiological Parameters /EEG, DC and Tissue Available O2/ and Regional Metabolites /pH, ATP, Glucose, NADH, K/ after 45 Min MCA Occlusion and 3 Hours Recirculation in Cats

      • L. Csiba, D. Bereczki, W. Paschen, F. Linn

      Pages 137-138

   6. Cerebral Hypoxia during Repetitive Seizures

      • Norman R. Kreisman

      Pages 139-149

   7. Microcirculation, NAD/NADH Fluorescence, Extracellular Potassium and Glucose Metabolism Changes in Focal Cerebral Ischemia

      • Rudolf Urbanics, Joel H. Greenberg, Martin Reivich

      Pages 151-152

   8. Neurons, Glia and Ions in Hypoxia, Hypercapnia and Acidosis

      • Alfred Lehmenkühler, Heinz Caspers, Erwin-Josef Speckmann, Dieter Bingmann, Hans G. Lipinski, Ulrich Kersting

      Pages 153-164

   9. Effects of Anoxia on Nerve Cell Function

      • Anker Jon Hansen

      Pages 165-173

The articles and short communications in this volume are based on papers pre­ sented to the Symposium on Cerebral Hypoxia and Stroke held in Budapest in August of 1987. Besides participants at the meeting, three scientists who were invited but could not attend have also contributed chapters to this volume. A synopsis of the general discussion at the conference and a review chapter conclude this volume. To the readers of this book it will not be news that stroke is a worldwide problem. Efforts to cope with this often devastating condition are worldwide also, as attested by the international membership of the conference. It has been said of oxygen deficiency that it not only stops the machine, it also wrecks the machinery. The paramount question in stroke research is this: why can't the brain be restarted after a hypoxic episode in much the same manner as a motor car can when its gas tank is refilled after it stalled because it ran out of fuel? Participants at the Symposium had been requested in advance of the meeting to especially consider a series of specific questions in relation to this general problem. Among these specific questions were: the mechanism of synaptic blockade in hypoxic brain tissue; the transition from reversible to irreversible arrest of function; the nature of postischemic (delayed) cell death; the possible basic differences in the consequences of hypoxia and ischemia; and actual and potential approaches to the prevention and treatment of cell damage in hypoxia and stroke.

• brain
• cell
• cell death
• cortex
• oxygen
• paper
• physiology
• receptor
• tissue

• Duke University Medical Center, Durham, USA

  George Somjen

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