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Valproic acid induces prosurvival transcriptomic changes in swine subjected to traumatic injury and hemorrhagic shock.

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BACKGROUND Valproic acid (VPA) is a histone deacetylase inhibitor that improves outcomes in large animal models of trauma. However, its protective mechanism of action is not completely understood. We sought to characterize the genetic changes induced by VPA treatment following traumatic

Valproic Acid Attenuates the Risk of Acute Respiratory Failure in Patients with Subarachnoid Hemorrhage.

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UNASSIGNED Valproic acid (VPA) has shown potent anti-inflammatory effect and attenuates acute lung injury. UNASSIGNED To determine whether the use of VPA is associated with a decreased risk of acute respiratory failure (ARF) in patients with subarachnoid hemorrhage (SAH). UNASSIGNED The Taiwan

Valproic acid-associated low fibrinogen and delayed intracranial hemorrhage: case report and mini literature review.

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A 41-year-old male had suffered from gradual hearing loss in his right ear for 2 years. Head computed tomography and magnetic resonance imaging scans showed a neoplasm in the cerebellopontine angle region, which was confirmed by the diagnosis of acoustic neurilemmoma by pathological findings after

Hepatoprotection and lethality rescue by histone deacetylase inhibitor valproic acid in fatal hemorrhagic shock.

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BACKGROUND Pharmacological histone deacetylase (HDAC) inhibitors, such as known anticonvulsant valproic acid (VPA), demonstrate cytoprotective effects and increase acetylation of nuclear histones, promoting transcriptional activation of deregulated genes. Therefore, we examined protective effects of

Valproic acid prevents hemorrhage-associated lethality and affects the acetylation pattern of cardiac histones.

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Pharmacological inhibitors of histone deacetylases (HDAC) demonstrate cytoprotective effects both in vitro and in vivo. In this study, we investigated whether valproic acid (VPA), a known mood stabilizer and anticonvulsant with HDAC-inhibiting activity, improves survival following otherwise lethal

Image in toxicology: Pseudo-subarachnoid hemorrhage in a case of severe valproic acid poisoning.

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Pseudo-subarachnoid hemorrhage (PSAH) is a false-positive finding on cranial computed tomography (CT) in patients with cerebral edema. Its appearance on CT resembles subarachnoid hemorrhage despite the absence of subarachnoid blood. We report the finding of PSAH in a case of massive valproic acid

Treatment with a histone deacetylase inhibitor, valproic acid, is associated with increased platelet activation in a large animal model of traumatic brain injury and hemorrhagic shock.

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BACKGROUND We have previously shown that resuscitation with fresh frozen plasma (FFP) in a large animal model of traumatic brain injury (TBI) and hemorrhagic shock (HS) decreases the size of the brain lesion, and that addition of a histone deacetylase inhibitor, valproic acid (VPA), provides

Valproic acid for the treatment of hemorrhagic shock: a dose-optimization study.

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BACKGROUND Valproic acid (VPA) has been shown to improve survival in animal models of hemorrhagic shock at a dose of 300 mg/kg. Our aim was to identify the ideal dose through dose-escalation, split-dosing, and dose de-escalation regimens. METHODS Rats were subjected to sublethal 40% hemorrhage and

Valproic acid-mediated myocardial protection of acute hemorrhagic rat via the BCL-2 pathway.

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BACKGROUND Hemorrhage is a major cause of morbidity and mortality among trauma patients. The pathophysiologic changes following acute severe hemorrhage and tissue hypoxia lead to an imbalance of protein acetylation. Histone deacetylase inhibitors (HDACIs) were reported to restore the acetylation

Hypothermia and valproic acid activate prosurvival pathways after hemorrhage.

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BACKGROUND Therapeutic hypothermia (hypo) and valproic acid (VPA, a histone deacetylase inhibitor) have independently been shown to be protective in models of trauma and hemorrhagic shock but require logistically challenging doses to be effective. Theoretically, combined treatment may further

[The effects of administration of valproic acid on organ function and outcome in a canine lethal hemorrhagic shock model].

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OBJECTIVE To investigate the effects of valproic acid (histone deacetylase inhibitor) on visceral function and outcome in a canine lethal hemorrhage model. METHODS Twenty male Beagle canines were subjected to an about 42% of total blood volume loss to reproduce a lethal hemorrhage shock model.

Identification of a novel potential biomarker in a model of hemorrhagic shock and valproic acid treatment.

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BACKGROUND The initial management of a poly-trauma patient requires evaluation for potential hemorrhage and ongoing monitoring to assess the efficacy of treatment and avoid complications related to massive blood loss. Certain serum protein levels may be altered in response to hemorrhagic shock, and

Diffuse alveolar hemorrhage due to valproic acid: Case report and review of the literature.

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Valproic acid (VPA) is one of the most frequently used antiepileptic drugs for the treatment of focal and generalized epilepsies, absence seizures, and Lennox-Gastaut syndrome (LGS). VPA has been demonstrated to have a negative effect on both the intrinsic and extrinsic coagulation systems and

Resuscitation with Valproic Acid Alters Inflammatory Genes in a Porcine Model of Combined Traumatic Brain Injury and Hemorrhagic Shock.

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Traumatic brain injury and hemorrhagic shock (TBI+HS) elicit a complex inflammatory response that contributes to secondary brain injury. There is currently no proven pharmacologic treatment for TBI+HS, but modulation of the epigenome has been shown to be a promising strategy. The aim of this study

Valproic acid protects against haemorrhagic shock-induced signalling changes via PPARγ activation in an in vitro model.

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OBJECTIVE Valproic acid (VPA), a widely used epilepsy and bipolar disorder treatment, provides acute protection against haemorrhagic shock-induced mortality in a range of in vivo models through an unknown mechanism. In the liver, this effect occurs with a concomitant protection against a decrease in

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