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arachidonic acid/hypoxia
Odkaz sa uloží do schránky
Strana 1 od 425 výsledky
Arachidonic acid potentiates hypoxia-induced VEGF expression in mouse embryonic stem cells: involvement of Notch, Wnt, and HIF-1alpha.
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Recent investigations suggest that hypoxia increases the release of fatty acids, which participate in the regulation of cytokine synthesis and cell growth. Therefore, in this study, we examined the effect of arachidonic acid (AA) on hypoxia-induced vascular endothelial growth factor (VEGF)
Effect of hypoxia and dopamine on arachidonic acid metabolism in superior cervical ganglion.
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Superior cervical ganglion (SCG) may play a modulatory role on ventilatory control through its efferent sympathetic fibres, which innervate cells in the carotid bodies. In this study the in vivo effect of acute hypoxia versus normoxia on arachidonic acid (AA) metabolism was investigated in cat SCG.
Effect of arachidonic acid metabolic inhibitors on hypoxia/reoxygenation-induced renal cell injury.
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The present study was undertaken to examine the role of arachidonic acid (AA) metabolites in hypoxia/reoxygenation (H/R)-induced renal cell injury in rabbit renal cortical slices using AA metabolic inhibitors. Inhibitors of cyclooxygenase (indomethacin and diclofenac sodium) and lipoxygenase
Endogenous arachidonic acid metabolism by calcium ionophore stimulated ferret lungs. Effect of age, hypoxia.
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We have studied the metabolism of endogenous arachidonic acid by isolated perfused lungs of ferrets when stimulated with calcium ionophore A23187 at two ages, neonatal (2- to 3-week-old) and adult (greater than 6 months). We have also determined the effect of hypoxia on lung metabolism of
Metabolism of endogenous arachidonic acid by isolated lungs of neonatal and adult rabbits stimulated with calcium ionophore: effect of hypoxia.
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We have determined the effect of hypoxia on arachidonic acid metabolism by rabbit lungs stimulated with calcium ionophore A23187. Isolated lungs of neonatal and adult rabbits were perfused during normoxia (pO2 greater than 100 torr) or hypoxia (pO2 less than 40 torr) and arachidonic acid metabolism
Arachidonic acid participates in the anoxia-induced increase in mEPSC frequency in CA1 neurons of the rat hippocampus.
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Patch clamp in the whole cell configuration was used to examine the effects of a variety of agents that influence arachidonic acid metabolism on vesicular glutamate release in CA1 neurons of rat hippocampal slices. As previously demonstrated, anoxia induced a significant increase in the frequency of
Short-period hypoxia increases mouse embryonic stem cell proliferation through cooperation of arachidonic acid and PI3K/Akt signalling pathways.
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Hypoxia plays important roles in some early stages of mammalian embryonic development and in various physiological functions. This study examined the effect of arachidonic acid on short-period hypoxia-induced regulation of G(1) phase cell-cycle progression and inter-relationships among possible
Effect of arachidonic acid on hypoxia-induced IL-6 production in mouse ES cells: Involvement of MAPKs, NF-kappaB, and HIF-1alpha.
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This study examined the role of arachidonic acid (AA) in hypoxia-induced production of interleukin (IL)-6 and its related signaling pathways in mouse embryonic stem (ES) cells. Hypoxia with AA induced IL-6 production, which was mediated by reactive oxygen species (ROS). In addition, hypoxia
The influence of nimodipine and MK-801 on the brain free arachidonic acid level and the learning ability in hypoxia-exposed rats.
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1. The influence of voltage dependent calcium channel blocker (VDCC), nimodipine and N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 on the brain free arachidonic acid (FAA) level and on the learning ability in hypoxia-exposed rats was examined. 2. Some animals were decapitated after
Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis.
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Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the
The influence of nicardipine and ifenprodil on the brain free arachidonic acid level and behavior in hypoxia-exposed rats.
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1. The effects of the calcium channel blockers, nicardipine and ifenprodil, on the brain free arachidonic acid level and learning ability in rats exposed to hypoxia were examined. 2. Adult rats were injected with 0.003; 0.01; 0.03; 0.1; 0.3 or 1.0 mg/kg of tested drugs i.p. Thirty min later the
Inhibition effect of arachidonic acid on hypoxia-induced [Ca(2+)](i) elevation in PC12 cells and human pulmonary artery smooth muscle cells.
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[Ca(2+)](i) elevation is a key event when O(2) sensitive cells, e.g. PC12 cells and pulmonary artery smooth muscle cells, face hypoxia. Ca(2+) entry pathways in mediating hypoxia-induced [Ca(2+)](i) elevation include: voltage-gated Ca(2+) channels (VGCCs), transient receptor potential (TRP) channel
Regulation of rat intrapulmonary arterial tone by arachidonic acid and prostaglandin E2 during hypoxia.
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OBJECTIVE
Arachidonic acid (AA) and its metabolites, prostaglandins (PG) are known to be involved in regulation of vascular homeostasis including vascular tone and vessel wall tension, but their potential role in Hypoxic pulmonary vasoconstriction (HPV) remains unclear. In this study, we examined
Perinatal pulmonary responses to arachidonic acid during normoxia and hypoxia.
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Dilator prostaglandins are released from the perinatal lung in response to ventilation and also may be involved in the pressor response to hypoxia. However, arachidonic acid, precursor of bisenoic prostaglandins, causes pulmonary vasoconstriction when infused into the pulmonary circulation of
Effect of hypoxia on steady-state arachidonic acid metabolism in bovine aortic endothelial cells.
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At the onset of acute hypoxia, eicosanoid synthesis by bovine aortic endothelial cells (BAEC) markedly decreases, reflecting a decreased release of arachidonic acid from endogenous stores. To determine the cause of decreased arachidonic acid release, we pulse-labeled BAEC with [14C]arachidonic acid
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