hydrogen sulfide/edema

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α-ENaC, a therapeutic target of dexamethasone on hydrogen sulfide induced acute pulmonary edema.

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Acute pulmonary edema (APE) is one of the fatal outcomes after exposure to high levels of hydrogen sulfide (H2S), available evidence suggest that dexamethasone (DXM), a potent anti-inflammatory agent, has been widely used or proposed as a therapeutic approach for H2S-induced APE in clinical

Hydrogen sulfide inhalation decreases early blood-brain barrier permeability and brain edema induced by cardiac arrest and resuscitation.

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The effects of hydrogen sulfide (H2S) on blood-brain barrier (BBB) and brain edema after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remain poorly understood. We investigated the effects of exogenous 80-p.p.m. H2S gas on BBB, brain water content, neurologic outcome, and survival rate

Hydrogen sulfide attenuates brain edema in early brain injury after subarachnoid hemorrhage in rats: Possible involvement of MMP-9 induced blood-brain barrier disruption and AQP4 expression.

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This study investigated the effect of H2S on brain edema formation and the possible underlying mechanisms in early brain injury (EBI) of SAH using the endovascular perforation model. 96 male rats were randomly divided into four groups: sham group, SAH+vehicle group, SAH+low-dosage NaHS group, and

[Toxic pulmonary edema after inhalation of hydrogen sulfide. Successful treatment by continuous positive pressure ventilation].

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Bronchial injury and pulmonary edema caused by hydrogen sulfide poisoning.

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Neuroprotective Effects of Hydrogen Sulfide Against Early Brain Injury and Secondary Cognitive Deficits Following Subarachnoid Hemorrhage.

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Although the neuroprotective effects of hydrogen sulfide (H2 S) have been demonstrated in several studies, whether H2 S protects against early brain injury (EBI) and secondary cognitive dysfunction in subarachnoid hemorrhage (SAH) model remains unknown. This study was undertaken to evaluate the

A fatality caused by accidental production of hydrogen sulfide.

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A 55-year-old male Caucasian truck driver was dead at the scene after breathing hydrogen sulfide (H(2)S) produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H(2)SO(4)) and iron(II) sulfate (FeSO(4)). Autopsy of the

[The impact of hydrogen sulfide on the heme oxygenase-1/carbon monoxide system in Coxsackie virus B3-induced myocarditis in mice].

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Objective: To explore the impact of hydrogen sulfide (H(2)S) on the heme oxygenase-1/carbon monoxide pathway in Coxsackie virus B3 (CVB3)-induced murine myocarditis (VMC) model. Method: A total of 70 inbred male Balb/c mouse (4-6 weeks old) were randomized into the following four groups: Normal,

Gastrointestinal safety and anti-inflammatory effects of a hydrogen sulfide-releasing diclofenac derivative in the rat.

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OBJECTIVE Gastrointestinal damage caused by nonsteroidal anti-inflammatory drugs (NSAIDs) remains a significant clinical problem. Hydrogen makes an important contribution to mucosal defense, and NSAIDs can suppress its synthesis. In this study, we evaluated the gastrointestinal safety and

Are anti-inflammatory properties of lipoic acid associated with the formation of hydrogen sulfide?

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BACKGROUND Lipoic acid (LA) was shown to possess anti-inflammatory properties. In this study, we present evidence supporting the hypothesis that the anti-inflammatory properties of LA are associated with the formation of hydrogen sulfide (H2S). METHODS The study was conducted on male albino Swiss

Brain damage caused by hydrogen sulfide: a follow-up study of six patients.

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Hydrogen sulfide (H2S) poisoning involves a risk of hypoxic brain damage. Six patients who lost consciousness due to H2S poisoning are described. The symptoms varied from anosmia in the patient with the shortest but highest exposure to delayed neurological deterioration in the patient with the

[Mechanism research and effect of ulinastatin in the brain tissue injury of acute hydrogen sulfide intoxicated rats].

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OBJECTIVE To observe the effect of Ulinastatin (UTI) in the dynamic changes of aquaporin 4 (AQP4) and cyclooxygenase-2 (COX-2) in the brain tissue injury of acute hydrogen sulfide (H2S) intoxicated, to explore the Mechanism of brain tissue injury of acute H2S-intoxicated and the protection effect of

Acute pit gas (hydrogen sulfide) poisoning in confinement cattle.

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Rapid deaths in confinement cattle caused by exposure to hydrogen sulfide (H2S) gas from manure pits has not been reported in the USA. In 1997, 158 cattle in 2 confinement pens were exposed to H2S gas as the manure in the pits under a slatted floor was agitated prior to pumping. Approximately 35 of

Effect of the Inhibition of Hydrogen Sulfide Synthesis on Ischemic Injury and Oxidative Stress Biomarkers in a Transient Model of Focal Cerebral Ischemia in Rats.

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OBJECTIVE Hydrogen sulfide (H2S) plays multiple roles in the function of the central nervous system in physiological and pathological conditions, such as cerebral ischemia. Recent studies have reported controversial results about the role of H2S in cerebral ischemia. The aim of this study was to

Hydrogen sulfide intoxication.

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Hydrogen sulfide (H2S) is a hazard primarily in the oil and gas industry, agriculture, sewage and animal waste handling, construction (asphalt operations and disturbing marshy terrain), and other settings where organic material decomposes under reducing conditions, and in geothermal operations. It

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