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Hypoxia-ischemia

A number of toxic conditions beside hypoosmotic stress and hypoxia/ischemia produce brain edema and the causes may be related to regulation of the aquaporins (see Ch. 34). AQP1 and AQP4 are intensely upregulated in reactive astrocytes in subarachnoid hemorrhage [69], in human glioma and astrocytoma [70] and AQP4 in endothelia and reactive astrocytes in metastatic carcinoma [71,72]. [Pg.90]

Blumberg, R. M., Cady, E. B., Wigglesworth, J. S. etal. Relation between delayed impairment of cerebral metabolism and infarction following transient focal hypoxia-ischemia in the developing brain. Exp. Brain Res. 113 130-137, 1997. [Pg.557]

Energy failure, an early consequence of hypoxia-ischemia, causes disruption of ionic homeostasis and accumulation of extracellular neurotransmitters 559... [Pg.559]

Hypoxia-ischemia disrupts the blood-brain barrier and damages endothelial cells 562... [Pg.559]

Excitatory amino acid-receptor antagonists can provide neuroprotection in experimental models of hypoxia-ischemia 565... [Pg.559]

Hypoxia-ischemia may initiate apoptosis in parallel with excitotoxicity 565 Triggers of ischemic apoptosis may include decreased supply or sensitivity to neurotrophins, oxidative stress, exposure to inflammatory cytokines or damage to mitochondria 566... [Pg.559]

Thrombolytics and drugs targeting several injury pathways have shown efficacy in models of hypoxia—ischemia 571... [Pg.559]

Hypoxia-ischemia disrupts the blood-brain barrier and damages endothelial cells. Damage to the blood-brain barrier (BBB), which occurs gradually following isch-emia-reperfusion, reflects the vulnerability of the cellular... [Pg.562]

Excitotoxicity leads to increased Ca2+ and Zn2+, which can activate cytotoxic intracellular pathways. The prolonged availability of extracellular glutamate during hypoxia-ischemia is transduced by neuronal membrane receptors into potentially lethal intracellular ionic derangements, in particular, intracellular Na+ and Ca2+ overload. Excitotoxic... [Pg.564]

Thrombolytics and drugs targeting several injury pathways have shown efficacy in models of hypoxia-ischemia. A number of neuroprotective strategies have been identified in animal models of ischemia, and many... [Pg.571]

See other pages where Hypoxia-ischemia is mentioned: [Pg.350]    [Pg.288]    [Pg.306]    [Pg.559]    [Pg.559]    [Pg.559]    [Pg.559]    [Pg.559]    [Pg.560]    [Pg.562]    [Pg.563]    [Pg.563]    [Pg.565]    [Pg.565]    [Pg.565]    [Pg.566]    [Pg.566]    [Pg.566]    [Pg.571]   
See also in sourсe #XX -- [ Pg.350 ]

See also in sourсe #XX -- [ Pg.559 , Pg.560 , Pg.561 , Pg.562 , Pg.563 , Pg.564 , Pg.565 , Pg.566 , Pg.567 , Pg.568 , Pg.569 , Pg.570 ]



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Antioxidants hypoxia-ischemia

Calcium hypoxia-ischemia

Cytokines hypoxia-ischemia

Excitotoxicity hypoxia-ischemia

Free radicals hypoxia-ischemia

Growth factors hypoxia-ischemia

HIF-1 Activation in Hypoxia and Ischemia During Aging

Hypoxia from ischemia

Hypoxia-ischemia apoptosis

Hypoxia-ischemia brain infarction

Hypoxia-ischemia edema

Hypoxia-ischemia energy failure

Hypoxia-ischemia excitotoxic injury

Hypoxia-ischemia oxidative stress

Hypoxia-ischemia reactive oxygen species

Hypoxia-ischemia receptors

Lipids hypoxia-ischemia

Neurotransmitters hypoxia-ischemia

Nitric oxide hypoxia-ischemia

Potassium hypoxia-ischemia

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