Brain Ischemia

1. Front Matter

   Pages i-xiv

   PDF

2. Introduction

   1. Introduction

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 1-5

3. Mechanisms of Ischemic Brain Damage

   1. Front Matter

      Pages 7-7

      PDF

   2. Hemodynamic Events Associated with Acute Focal Brain Ischemia and Reperfusion. Ischemic Penumbra

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 9-19

   3. Cellular Reactions in Response to Acute Focal Brain Ischemia

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 21-29

   4. Energy Failure Induced by Brain Ischemia

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 31-37

   5. The Glutamate—Calcium Cascade

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 39-93

   6. Metabolic Acidosis and Ischemic Damage

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 95-99

   7. Delayed Neuronal Death Following Acute Focal Brain Ischemia

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 101-102

   8. Gene Expression and Subsequent Molecular Events in Response to Acute Brain Ischemia

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 103-114

   9. Microglial Activation, Cytokine Production, and Local Inflammation in Focal Brain Ischemia

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 115-145

   10. Autoimmune Mechanisms of Trophic Dysfunction and Ischemic Brain Damage

       • Eugene Gusev, Veronica I. Skvortsova

       Pages 147-182

   11. Programmed Cell Death. Apoptosis in Focal Brain Ischemia

       • Eugene Gusev, Veronica I. Skvortsova

       Pages 183-205

   12. Reaction of the Stress-Mediating Endocrine System in Response to Acute Brain Ischemia

       • Eugene Gusev, Veronica I. Skvortsova

       Pages 207-217

   13. Molecular Mechanisms of Post-Ischemic Reparation Events

       • Eugene Gusev, Veronica I. Skvortsova

       Pages 219-226

4. Neuroprotection in Brain Ischemia

   1. Front Matter

      Pages 227-227

      PDF

   2. Modern Therapeutic Approaches to Acute Focal Brain Ischemia. Basic Strategies for Neuroprotection

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 229-236

   3. Primary Neuroprotection

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 237-284

   4. Secondary Neuroprotection

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 285-351

   5. Reparative Therapy

      • Eugene Gusev, Veronica I. Skvortsova

      Pages 353-368

Ischemia is localized tissue anemia due to obstruction of the inflow of arterial blood, thus brain ischemia is the condition where insufficient blood is delivered to the brain. Many physiological processes occurring in the brain critically depend on the state of its energy metabolism. The state of brain energy metabolism in turn depends on the delivery of oxygen and glucose to the brain via the bloodstream. Although it comprises only 2% of the total body weight, the human brain consumes 20-25% of the oxygen and up to 70% of the free glucose taken in by the body. The brain respires more intensively than any other organ of the body. The intensity of oxygen consumption by cortical brain tissue much exceeds the demands of other tissues (5.43 mmol 02/g per h versus 3.06 and 4.02 mmol for heart at rest and intensively working, respectively, 2.4 mmol for kidneys, and 1.8 mmol for liver). Oxidative phosphorylation in mitochondria generates 95% of the adenosine triphosphate (ATP) that is formed in the brain. Thus, it is clear why insufficiency of oxygen delivery to brain cells adversely affects brain function. Glucose is the main energy-providing substrate in the brain. The basic pathway of its metabolism in neural tissue is aerobic glycolysis.

• brain
• death
• depression
• glutamate receptor
• neuropeptides
• neuroprotection
• oxidative stress
• receptor
• stroke

• Russian State Medical University, Moscow, Russia

  Eugene Gusev, Veronica I. Skvortsova

Policies and ethics