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dimethyl sulfoxide/hypoxia
Veza se sprema u međuspremnik
Page 1 od 76 rezultati
Myocardial function during hypoxia: protective effect of dimethyl sulfoxide (DMSO).
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Electrically driven rabbit left atria were exposed to 20 min periods of hypoxia in the presence and absence of dimethyl sulfoxide (DMSO) or sucrose. Contractile strength declined significantly less than control when tissues were exposed to DMSO during hypoxia. On reoxygenation tissues treated with
Myocardial function during hypoxia: effects of dimethyl sulfoxide (DMSO) and different buffers.
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Isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin.
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BACKGROUND
Volatile anesthetics are known to protect the heart against ischemia-reperfusion injury. The authors tested whether anesthetic preconditioning with isoflurane is mediated via activation of the transcription factor hypoxia inducible factor 1 (HIF-1) and evaluated the role of mammalian
Dimethyl sulfoxide in central nervous system trauma.
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Dimethyl sulfoxide has been tested in various experimental injuries of the central nervous system in relation to other therapies. It appears to be a useful drug in acute extradural mass-forming lesions, middle cerebral artery occlusion, respiratory anoxia, and spinal cord injuries, in rhesus and
Midazolam improves electrophysiologic recovery after anoxia and reduces the changes in ATP levels and calcium influx during anoxia in the rat hippocampal slice.
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Since blockers of excitatory transmission have been shown to reduce anoxic and ischemic neuronal damage, augmentation of inhibitory transmission by agents such as midazolam might have a similar protective effect. Rat hippocampal slices were maintained in vitro and used to determine whether and by
Recombinant human interleukin (IL)-1 beta-mediated regulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) stabilization, nuclear translocation and activation requires an antioxidant/reactive oxygen species (ROS)-sensitive mechanism.
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Cytokine-mediated regulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) non-hypoxic stabilization, translocation and activation is not well characterized. Furthermore, evidence that reactive oxygen species (ROS) signaling mediates interleukin (IL)-1 beta-dependent regulation of HIF-1 alpha
[Diazoxide preconditioning combined with subsequent hypothermia alleviates anoxia-re-oxygenation injury: experiment with rat hippocampal neurons].
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OBJECTIVE
To observe the alleviative effects of preconditioning with diazoxide (DZ), a mitochondrial ATP-sensitive potassium channel opener, combined with subsequent hypothermia on anoxia-re-oxygenation injury.
METHODS
Hippocampal neurons of new-born SD rat were cultured. DZ of the concentration of
Role of oxidative stress in hypoxia-reoxygenation injury to cultured rat hepatic sinusoidal endothelial cells.
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To characterize the role of oxidative stress in cultured rat sinusoidal endothelial cells, we studied the production of superoxide after reoxygenation, the relationship of reduced glutathione (GSH) levels to cell injury, and the protective efficacy of antioxidants. Hypoxia (pO(2) 1-2 mm Hg) was
Dimethyl sulfoxide increases latency of anoxic terminal negativity in hippocampal slices of guinea pig in vitro.
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Dimethyl sulfoxide (DMSO), which is widely used as a solvent for a variety of drugs, was used in the present study to investigate its ability to increase the hypoxic tolerance of brain tissue in vitro. DC-potentials and evoked potentials (EP, Schaffer collateral stimulation) were recorded in the CA1
Acute protective effect of nimodipine and dimethyl sulfoxide against hypoxic and ischemic damage in brain slices.
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Nimodipine and dimethyl sulfoxide (DMSO) were tested (alone and in combination) regarding their ability to increase hypoxic tolerance of brain slices under 'hypoxic' (deprivation of oxygen) or 'ischemic' (hypoxia+withdrawal of glucose) conditions. Direct current (DC) and evoked potentials were
Advanced retinoblastoma treatment: targeting hypoxia by inhibition of the mammalian target of rapamycin (mTOR) in LH(BETA)T(AG) retinal tumors.
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OBJECTIVE
The purpose of this study is to analyze the dose response of the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, on tumor burden and hypoxia, and study the treatment effect on vasculature in LH(BETA)T(AG) retinal tumors.
METHODS
This study was approved by the Institutional
[Effects of hypoxia inducible factor-1α on P311 and its influence on the migration of murine epidermal stem cells].
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Objective: To explore the effects of hypoxia inducible factor-1α (HIF-1α) on P311 and its influence on the migration of murine epidermal stem cells (ESCs) under hypoxia in vitro. Methods: Two kinds of murine ESCs were isolated and obtained from 15 neonatal wild-type C57BL/6J mice and 5 congeneric
Modeling Direct and Indirect Action on Cell Survival After Photon Irradiation under Normoxia and Hypoxia
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The demand for personalized medicine in radiotherapy has been met by a surge of mechanistic models offering predictions of the biological effect of ionizing radiation under consideration of a growing number of parameters. We present an extension of our existing model of cell survival after photon
[Effect of notoginsenoside Rg1 on p38MAPK expression of pulmonary arterial smooth muscle cells exposed to hypoxia hypercapnia].
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OBJECTIVE
To study the effect of Notoginsenoside Rgl on p38 mitogen activated protein kinase (p38MAPK) expression in pulmonary artery smooth muscle cells (PASMCs) cultured in hypoxia hypercapnia.
METHODS
SD rat PASMCs was primary cultured, the cells of passage 2- 5 were divided into six groups:
The protective effect of ceramide in immature rat brain hypoxia-ischemia involves up-regulation of bcl-2 and reduction of TUNEL-positive cells.
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Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway. A hypoxic-ischemic (HI) insult in the immature rat injures brain primarily through apoptosis.
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