Cerebral Ischemia

Molecular and Cellular Pathophysiology

Specificaties
Gebonden, 278 blz. | Engels
Humana Press | 1999e druk, 1999
ISBN13: 9780896035409
Rubricering
Humana Press 1999e druk, 1999 9780896035409
Onderdeel van serie Contemporary Neuroscience
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Samenvatting

The human brain represents about 2% of the body weight, yet it accounts for approximately 20% of aerobic metabolism. This high dependency on energy-consuming processes is mainly caused by the active transport of ions, which is necessary to compensate for the transmembrane ion currents that are part ofthe complex signaling processes in the brain. Ninety-five percent ofthe brain's ATP is derived from mitochondrial oxidative phosphorylation. Since that organ' s storage capacity for oxygen is minimal, any interruption of oxygen delivery to brain cells willlead to changes in membrane excitability and, there­ fore, to disruption of neuronal signaling within seconds. It seems that mamma­ lian brain is especially vulnerable to such an interruption, since oxygen deprivation leads to activation of ion channel mechanisms in neurons that impair their communications. Thus, the function of the brain as a coordinator of vital homeostatic reflexes, and complex body reactions to external challenges, depends critically on the rate of oxygen delivery and oxygen consumption. Oxygen delivery depends on two variables described in the Fick relation­ ship: volume flow rate ofblood and the arterial oxygen content. A reduction in either of these two variables will have serious effects on vital brain func­ tions. Reduction of arterial blood flow to the brain can be caused by cardiac arrest, shock, carotid occlusion, Of hypotension (global ischemia). Oxygen content is progressively decreased in asphyxia (including drowning).

Specificaties

ISBN13:9780896035409
Taal:Engels
Bindwijze:gebonden
Aantal pagina's:278
Uitgever:Humana Press
Druk:1999

Inhoudsopgave

1 Mechanisms of Cerebral Ischemic Damage.- 2 Spreading Depression Waves as Mediators of Secondary Injury and of Protective Mechanisms.- 3 Cell Swelling in Cerebral Ischemia.- 4 Calcium Overload.- 5 Oxygen Radicals.- 6 Mechanisms of Neuroprotective Cytokines: Pleiotrophic Effects of TNF? and TGF? on Brain Injury.- 7 Reprogramming of Gene Expression After Ischemia.- 8 Neurons: Necrotic vs Apoptotic Changes.- 9 Reactive Astrogliosis in the Injured and Postischemic Brain.- 10 Activated and Phagocytic Microglia.
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        Cerebral Ischemia