heart arrest/phosphatase

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Activation of brain protein phosphatase-1(I) following cardiac arrest and resuscitation involving an interaction with 14-3-3 gamma.

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The intracellular signaling mechanisms that couple transient cerebral ischemia to cell death and neuroprotective mechanisms provide potential therapeutic targets for cardiac arrest. Protein phosphatase (PP)-1 is a major serine/threonine phosphatase that interacts with and dephosphorylates critical

Alkaline Phosphatase Treatment of Acute Kidney Injury in an Infant Piglet Model of Cardiopulmonary Bypass with Deep Hypothermic Circulatory Arrest.

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Acute kidney injury (AKI) is associated with prolonged hospitalization and mortality following infant cardiac surgery, but therapeutic options are limited. Alkaline phosphatase (AP) infusion reduced AKI in phase 2 sepsis trials but has not been evaluated for cardiac surgery-induced AKI. We developed

Protein phosphatase-2A is activated in pig brain following cardiac arrest and resuscitation.

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Protein phosphatase-2A (PP-2A) interacts with several regulators of cell death pathways and is therefore a potential component of signaling pathways linking global cerebral ischemia to cell death. Using a novel procedure to quantify PP-2A activity, we find that cardiac arrest with resuscitation and

Tissue alkaline phosphatase activity and expression in an experimental infant swine model of cardiopulmonary bypass with deep hypothermic circulatory arrest

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Background: Infant cardiac surgery with cardiopulmonary bypass results in decreased circulating alkaline phosphatase that is associated with poor postoperative outcomes. Bovine intestinal alkaline phosphatase infusion represents a novel

Early glycogen synthase kinase-3β and protein phosphatase 2A independent tau dephosphorylation during global brain ischaemia and reperfusion following cardiac arrest and the role of the adenosine monophosphate kinase pathway.

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Abnormal tau phosphorylation (p-tau) has been shown after hypoxic damage to the brain associated with traumatic brain injury and stroke. As the level of p-tau is controlled by Glycogen Synthase Kinase (GSK)-3β, Protein Phosphatase 2A (PP2A) and Adenosine Monophosphate Kinase (AMPK), different

Alkaline Phosphatase in Infant Cardiopulmonary Bypass: Kinetics and Relationship to Organ Injury and Major Cardiovascular Events.

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OBJECTIVE To determine the kinetics of alkaline phosphatase (AP) activity and concentration after infant cardiopulmonary bypass, including isoform-specific changes, and to measure the association between postoperative AP activity and major postoperative cardiovascular events, organ

Gender differences in 24-hour outcome following resuscitation after 9 minutes of cardiac arrest in dogs.

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OBJECTIVE To examine possible gender-specific differences in 24-hr outcome following resuscitation from 9 mins of controlled cardiac arrest. METHODS Preclinical, prospective study comparing two similarly prepared, independent control groups (one female group, one male group) included in a larger

Overexpression of MicroRNA-106b-5p Attenuates Kidney Injuries after Deep Hypothermic Circulatory Arrest in Rats.

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MicroRNAs (miRNA) have been identified to exert a wide range of biological functions in acute kidney injury (AKI) after deep hypothermic circulatory arrest (DHCA). We sought to investigate the renoprotection of miRNA-106b-5p in a rat model of DHCA by targeting phosphatase and tensin homolog

Paradoxical effects of cardiac arrest by multidose potassium cardioplegia on myocardial lysosome integrity and phospholipid content.

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Multidose potassium cardioplegia is known to result in greater preservation of myocardial ATP content and better recovery of function as compared to cardiac arrest induced by aortic clamping. The present study was undertaken to assess the effects of this procedure on biochemical markers of tissue

Hematologic and chemical changes observed during and after cardiac arrest in a canine model--a pilot study.

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OBJECTIVE To evaluate the effect of cardiac arrest and cardiopulmonary resuscitation (CPR) on blood chemistry in a canine model. METHODS Evaluative canine animal study. METHODS Animal laboratory accredited by the Association for Assessment and Accreditation of Laboratory Animals. METHODS Twenty-six

Brain enzyme changes as markers of brain damage in rat cardiac arrest model. Effects of corticosteroid therapy.

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Apneic asphyxia to cardiac arrest (CA) in rats of 10 min was reversed by cardiopulmonary resuscitation (CPR), and after controlled ventilation and controlled normotension for 20 min, was followed by decapitation and brain freezing, and determination of brain concentrations of cytosolic and lysosomal

Biologically variable bypass reduces enzymuria after deep hypothermic circulatory arrest.

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BACKGROUND Renal injury is common after open-heart surgery. Cardiopulmonary bypass contributes to the problem. We compared conventional nonpulsatile perfusion (NP) to biologically variable perfusion (BVP), which uses a computer controller to restore physiological beat-to-beat variability to roller

Eukaryotic initiation factor 2alpha kinase and phosphatase activity during postischemic brain reperfusion.

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When ischemic brain is reperfused, there is in vulnerable neurons immediate inhibition of protein synthesis associated with a large increase in phosphorylation of the alpha-subunit of eukaryotic initiation factor 2 [eIF2alpha, phosphorylated form eIF2alpha(P)]. We examined eIF2alpha kinase and

Alkaline phosphatase activity after cardiothoracic surgery in infants and correlation with post-operative support and inflammation: a prospective cohort study.

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BACKGROUND Limited evidence suggests that serum alkaline phosphatase activity may decrease after cardiac surgery in adults and children. The importance of this finding is not known. Recent studies, however, have identified a potential role for alkaline phosphatase as modulator of inflammation in

Induction of MAPK phosphatase-1 by hypothermia inhibits TNF-alpha-induced endothelial barrier dysfunction and apoptosis.

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OBJECTIVE Hypothermia therapy has been shown to confer robust protection against brain injury and cardiac arrest. However, the mechanisms underlying endothelial cell protection of hypothermia have not yet been completely elucidated. Here, we investigated molecular effects of hypothermia on tumour

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