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heart arrest/tyrosine
Веза се чува у привремену меморију
Страна 1 од 39 резултати
Regulation of tyrosine protein kinase receptor Trk-B and motor function in rats following cardiac arrest.
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Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. Sixty days later, the motor function of the animals was restored. In the present study, we investigated brain levels of tyrosine protein kinase receptor Trk-B with quantitative immunoblot
Therapeutic hypothermia attenuates brain edema in a pig model of cardiac arrest: Possible role of the angiopoietin-Tie-2 system.
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OBJECTIVE
This study aimed to clarify whether therapeutic hypothermia protects against cerebral edema following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) in a porcine model via regulating the angiopoietin-Tie-2 ligand-receptor system.
METHODS
Male pigs were randomized into the
Detoxification with hemabsorption after cardiac arrest does not improve neurologic recovery. Review and outcome study in dogs.
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We and others hypothesized that noxious substances released after prolonged cardiac arrest from malfunctioning liver, kidneys, or intestine (e.g. bacterial toxins, aromatic amino acids), might hamper recovery of the brain. The highly detoxifying effect of hemabsorption (i.e. hemoperfusion) with
Cardiovascular toxicity associated with small molecule tyrosine kinase inhibitors currently in clinical use.
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BACKGROUND
Tyrosine kinase inhibitors (TKIs) have changed the concepts of systemic therapy for a variety of advanced solid and hematologic malignancies. However, their toxicity can be significant, and includes both cardiac and non-cardiac effects.
METHODS
The authors evaluate comprehensively the
Comparison of low-flow cardiopulmonary bypass and circulatory arrest on brain oxygen and metabolism.
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BACKGROUND
In the neonatal brain we measured oxygen (Bo(2)), extracellular striatal dopamine (DA), and striatal tissue levels of ortho-tyrosine (o-tyr) during low-flow cardiopulmonary bypass (LFCPB) or deep hypothermic circulatory arrest (DHCA) and the post-bypass recovery period.
METHODS
Newborn
Effect of granulocyte-colony stimulating factor on expression of selected proteins involved in regulation of apoptosis in the brain of newborn piglets after cardiopulmonary bypass and deep hypothermic circulatory arrest.
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OBJECTIVE
The study objective was to investigate the effect of granulocyte-colony stimulating factor on the expression of proteins that regulate apoptosis in newborn piglet brain after cardiopulmonary bypass and deep hypothermic circulatory arrest.
METHODS
The newborn piglets were assigned to 3
Protein tyrosine phosphorylation in the ischemic brain.
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Cerebral ischemia, a pathological condition in which brain tissue experiences a shortage of cerebral blood flow, is associated with cerebrovascular disease, brain trauma, epilepsy, and cardiac arrest. A reduction in blood flow leaves the brain tissue unsupplied with oxygen and glucose, thus leading
Insulin induces tyrosine phosphorylation of a 90-kDa protein during postischemic brain reperfusion.
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Rat brain nuclear proteins were examined for tyrosine phosphorylation after resuscitation from a 10-min cardiac arrest. Insulin (1 unit/kg intravenously), given immediately after resuscitation, caused a marked increase in tyrosine phosphorylation of a 90-kDa brain protein. This effect occurred
Effects of NaHS and hydroxylamine on the expressions of brain-derived neurotrophic factor and its receptors in rats after cardiac arrest and cardiopulmonary resuscitation.
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BACKGROUND
H2S can also protect nerve cells. The objective of the study is to investigate the effects of hydrogen sulfide (H2S) on the expressions of brain-derived neurotrophic factor (BDNF) and its receptors, tyrosine protein kinase B (TrkB) and p75Hypothermic reperfusion after cardiac arrest augments brain-derived neurotrophic factor activation.
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Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest.
Increases in striatal and hippocampal impedance and extracellular levels of amino acids by cardiac arrest in freely moving rats.
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The time course of changes in the tissue impedance and the levels of extracellular transmitter and non-transmitter amino acids was studied in the striatum and hippocampus of the unanesthetized rat after cardiac arrest. Electrodes were implanted for the continuous measurement of tissue impedance so
Selection of reference genes for quantitative real-time PCR in a rat asphyxial cardiac arrest model.
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BACKGROUND
Cardiac arrest, and the associated arrest of blood circulation, immediately leads to permanent brain damage because of the exhaustion of oxygen, glucose and energy resources in the brain. Most hippocampal CA1 neurons die during the first week post the insult. Molecular data concerning the
Early mitochondrial dysfunction in electron transfer activity and reactive oxygen species generation after cardiac arrest.
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OBJECTIVE
Mitochondrial biology appears central to many conditions that progress to death but remains poorly characterized after cardiac arrest. Mitochondrial dysfunction in electron transfer and reactive oxygen species leakage during ischemia may lead to downstream events including mitochondrial
Src tyrosine kinase inhibition prevents pulmonary ischemia-reperfusion-induced acute lung injury.
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OBJECTIVE
Pulmonary ischemia-reperfusion is a pathological process seen in several clinical conditions, including lung transplantation, cardiopulmonary bypass, resuscitation for circulatory arrest, atherosclerosis, and pulmonary embolism. A better understanding of its molecular mechanisms is very
Activation of mitochondrial STAT-3 and reduced mitochondria damage during hypothermia treatment for post-cardiac arrest myocardial dysfunction.
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While therapeutic hypothermia improves the outcomes of individuals in cardiac arrest, the hemodynamic responses and mechanisms which underlie hypothermia-induced cardioprotection are not fully understood. Therefore, we investigated the mechanism by which induced hypothermia preserves cardiac
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