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colchicine/hypoxia
Länken sparas på Urklipp
Sida 1 från 52 resultat
[On erythroblast proliferation in stimulated erythropoiesis. Bone marrow studies on colchicine poisoned rats in hypoxia, after bleeding and after injection of erythropoietically active plasma (erythropoietin)].
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Influence of anoxia upon hematopoietic cells of tadpoles exposed to x-irradiation or colchicine.
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Differential Effects of Colchicine on Cardiac Cell Viability in an in vitro Model Simulating Myocardial Infarction.
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OBJECTIVE
We aimed to examine the effects of colchicine, currently in clinical trials for acute myocardial infarction (AMI), on the viability of cardiac cells using a cell line model of AMI.
METHODS
HL-1, a murine cardiomyocyte cell line, and H9C2, a rat cardiomyoblast cell line, were incubated with
Cytochalasin delays but does not prevent cell death from anoxia.
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The role of alterations in the cytoskeleton in the anoxic death of cultured hepatocytes was evaluated with the use of cytochalasin B and colchicine. The addition of 50 microM Cytochalasin did, however, reduce the rate of accumulation of dead cells but was without effect on the number of cells that
Multiple organ failure after an overdose of less than 0.4 mg/kg of colchicine: role of coingestants and drugs during intensive care management.
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BACKGROUND
Although the ingestion of a dose of colchicine lower than 0.5 mg/kg is usually complicated by a mortality rate less than 5%, severe complications may be associated with drug-drug interactions in case of overdose combining other drugs.
METHODS
A 33-year-old previously healthy woman was
Protective effects of colchicine in an experimental model of necrotizing enterocolitis in neonatal rats.
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BACKGROUND
The pathophysiology of necrotizing enterocolitis (NEC) includes the massive production of endogenous cytokines with exaggerated activation of inflammatory pathways. Colchicine has been used as an anti-inflammatory agent. The aim of this study was to investigate the possible beneficial
Cytoskeleton mediates inhibition of the fast Na+ current in respiratory brainstem neurons during hypoxia.
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Whole-cell Na+ currents (INa) were recorded in inspiratory neurons in a medullary slice preparation from neonatal mouse that contains the functional respiratory network. Hypoxia and metabolic poisoning with KCN rapidly inhibited INa by reducing the number of Na+ channels available for opening during
[The influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia].
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OBJECTIVE
To investigate the influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia.
METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A (with hypoxia), B (with hypoxia and administration of 10 micromol/ml
[The influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia].
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OBJECTIVE
To investigate the influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia.
METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A group (with hypoxia), B group (with hypoxia and administration of l0
Cardiac effects of hypoxia in the neotenous tiger salamander Ambystoma tigrinum.
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The aquatic form of the tiger salamander Ambystoma tigrinum lives in high-altitude ponds and is exposed to a hypoxic environment that may be either chronic or intermittent. In many animal species, exposure to hypoxia stimulates cardiac output and is followed by an increase in cardiac mass. The
[Effect of long-term adaptation of rats to hypoxia on the proliferation of bone marrow erythroid cells. I. An increase in cell flows and a decrease in the duration of mitosis].
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A 60 day adaptation of Wistar rats to hypoxia (six times a week, 6 hours a day) leads to: (1) the increase in cell flow from any phase of the erythroid cell life cycle to the next phase; (2) the change in the duration of the life cycle phases, corresponding to erythroblasts, basophilic normoblasts,
Both microtubule-stabilizing and microtubule-destabilizing drugs inhibit hypoxia-inducible factor-1alpha accumulation and activity by disrupting microtubule function.
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We have recently identified a mechanistic link between disruption of the microtubule cytoskeleton and inhibition of tumor angiogenesis via the hypoxia-inducible factor-1 (HIF-1) pathway. Based on this model, we hypothesized that other microtubule-targeting drugs may have a similar effect on
Microtubular stability affects cardiomyocyte glycolysis by HIF-1alpha expression and endonuclear aggregation during early stages of hypoxia.
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Hypoxia-inducible factor (HIF)-1alpha is a key regulator of anaerobic energy metabolism. We asked the following question: Does the breakdown of microtubular structures influence glycolysis in hypoxic cardiomyocytes by regulating HIF-1alpha? Neonatal rat cardiomyocytes were cultured under hypoxic
Adenosine in cerebral homeostatic role: appraisal through actions of homocysteine, colchicine, and dipyridamole.
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Mammalian neocortical tissues were incubated in [14C]adenine-containing fluids and their newly-synthesized adenine derivatives examined after periods of superfusion. Increased [K+] released adenine derivatives from the tissues, a release diminished by homocysteine. Homocysteine acted also to
[Effect of the microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia].
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OBJECTIVE
To investigate the effect of microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia.
METHODS
Myocardiocytes from Wistar rats were isolated according to routine procedure, and they were randomly divided into control group, depolymerization group (with
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