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Sida 1 från 153 resultat
Delayed memory dysfunction by transient hypoxia, and its prevention with forskolin.
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Rats exposed to 40 min hypoxia 3 h before a one-trial learning passive avoidance task showed impaired memory retention 24 h later. this model was used to assess the ability of forskolin to restore the delayed memory dysfunction. Significant amelioration of memory retention was observed when
The combination of forskolin and VPA increases gene expression efficiency to the hypoxia/neuron-specific system
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Background: Spinal cord injury (SCI) tends to damage neural tissue and generate a hypoxic environment. Studies have confirmed that single therapy with gene or stem cells is inefficient, but research into combining stem cells and gene
Altered myocardial Gs protein and adenylyl cyclase signaling in rats exposed to chronic hypoxia and normoxic recovery.
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The present work has analyzed the consequences of chronic intermittent high-altitude hypoxia for functioning of the G protein-mediated adenylyl cyclase (AC) signaling system in the right (RV) and left ventricular (LV) myocardium in rats. Adaptation to hypoxia did not appreciably affect the number of
Hypoxia and hyperoxia potentiate PAF receptor-mediated effects in newborn ovine pulmonary arterial smooth muscle cells: significance in oxygen therapy of PPHN.
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Platelet-activating factor (PAF) acting via its receptor (PAFR) is implicated in the pathogenesis of persistent pulmonary hypertension of the newborn (PPHN). Effects of long-term oxygen therapy on newborn lung are not well understood; therefore, we studied the effect of oxygen tension on ovine
Hypoxia alters expression and function of syncytin and its receptor during trophoblast cell fusion of human placental BeWo cells: implications for impaired trophoblast syncytialisation in pre-eclampsia.
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The fundamental process of placental trophoblast cell fusion (syncytiotrophoblast formation or syncytialisation) which is a characteristic of this tissue is poorly understood. Pre-eclampsia is associated with placental hypoxia and suppressed syncytiotrophoblast formation. We therefore have studied
Hypoxia-inducible factor 2 alpha impairs human cytotrophoblast syncytialization: New insights into placental dysfunction and fetal growth restriction
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Insufficient remodeling of uterine arteries causes pregnancy-related diseases, including fetal growth restriction and preeclampsia. In these situations, reduced maternal blood flow in the placenta is thought to be responsible for the persistence of a low oxygen environment throughout pregnancy. We
Effects of prolonged hypoxia on adenylate cyclase activity and beta-adrenergic receptors in pulmonary and systemic arteries of the rat.
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Prolonged hypoxia causes pulmonary hypertension but no change in systemic vasomotor tone. In an effort to define the mechanisms involved, we determined the effects of 3 and 7 days of hypoxia on adenylate cyclase activity and beta-adrenergic receptor binding characteristics in pulmonary and systemic
Morphological and functional alterations of the ductus arteriosus in a chicken model of hypoxia-induced fetal growth retardation.
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The hypoxic conditions in which children with intrauterine growth retardation (IUGR) develop are hypothesized to alter the development of the ductus arteriosus (DA). We aimed to evaluate the effects of in ovo hypoxia on chicken DA morphometry and reactivity. Hypoxia (15% O2 from day 6 to 19 of the
Differential regulation of the slow and rapid components of guinea-pig cardiac delayed rectifier K+ channels by hypoxia.
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The aim of this study was to examine the effects of acute hypoxia on the slow (I(Ks)) and rapid (I(Kr)) components of the native delayed rectifier K+ channel in the absence and presence of the beta-adrenergic receptor agonist isoproterenol (isoprenaline; Iso) using the whole-cell configuration of
Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.
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We explored the effects of two components of ischemia, hypoxia and glucose deprivation, on the beta-adrenergic receptor (beta AR)-adenylate cyclase system in a model of hypoxic injury in cultured neonatal rat ventricular myocytes. After 2 h of hypoxia in the presence of 5 mM glucose, cell surface
Effects of 5-day hypoxia on cardiac adrenergic neurotransmission in rats.
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Chronic hypoxia induces an overall sympathetic hyperactivation associated with a myocardial beta-receptor desensitization. The mechanisms involved in this desensitization were evaluated in 32 male Wistar rats kept in a hypobaric pressure chamber (PO2 = 40 Torr, atmospheric pressure = 450 Torr) for 5
Chronic in ovo hypoxia decreases pulmonary arterial contractile reactivity and induces biventricular cardiac enlargement in the chicken embryo.
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Although chronic prenatal hypoxia is considered a major cause of persistent pulmonary hypertension of the newborn, experimental studies have failed to consistently find pulmonary hypertensive changes after chronic intrauterine hypoxia. We hypothesized that chronic prenatal hypoxia induces changes in
Chronic hypoxia increases beta 1-adrenergic receptor mRNA and density but not signaling in neonatal rat cardiac myocytes.
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BACKGROUND
It is well recognized that the beta-adrenergic receptor-adenylylcyclase system is altered during myocardial ischemia/hypoxia. However, there are no data regarding either regulation of beta-adrenergic receptors, particularly at the mRNA level, or adenylylcyclase activity in isolated
Hypoxia decreases glucagon-like peptide-1 secretion from the GLUTag cell line.
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Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells
Contribution of prostaglandins in hypoxia-induced vasodilation in isolated rabbit hearts. Relation to adenosine and KATP channels.
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The mechanism of hypoxia-induced coronary vasodilation was studied in isolated, saline-perfused rabbit hearts under constant flow conditions. Reduction in the perfusion solution PO2 (from 520 +/- 6 to 103 +/- 9 mm Hg) under control conditions halved the coronary resistance and was accompanied by a
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