Hypoxia-ischemia receptors

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

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... 

D. Martin, N. Chinookoswong, and G. Miller, The Interleukin-1 Receptor Antagonist (rhlL-lra) Protects Against Cerebral Infarction in a Rat Model of Hypoxia-Ischemia, Experimental Neurology 130(1994)362-367. 

Tacrolimus capacity to blockade NO pathway is weU demonstrated. NO plays a major role in the pathogenesis of cerebral hypoxia-ischemia injury mediated by glutamate/N-methyl-D-aspartate (NDMA). This injury depends on intracellular calcium influx through NDMA receptor channels, which activate calcineurin with consequent dephosphorylation of constitutive NO synthase (cNOS). Tacrohmus addition to cultured neuronal cells reduced NDMA-mediated toxicity, through the inhibition of calcineurin activation, inhibition of cNOS dephosphorylation and consequent decrease in... 

Gurd, J. W., Bissoon, N., Beesley, P. W., Nakazawa, T., Yamamoto, T., and Vannucci, S. J. (2002). Differential effects of hypoxia-ischemia on subunit expression and tyrosine phosphorylation of the NMDA receptor in 7- and 21-day-old rats. J. Neurochem. 82, 848-856. 

A. Both dextromethorphan and its o-demethylated metabolite appear to antagonize /V-methyl-D-aspartate (NMDA) glutamate receptors, which may explain anticonvulsant properties and protection against hypoxia-ischemia observed in animal models. 

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

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