עמוד 1 מ 425 תוצאות
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)
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.
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
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
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
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
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
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
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
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
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
[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
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
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
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