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chlorine/hypoxie

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[Effects of hypoxia on plasma concentrations and daily elimination of sodium, potassium and chlorine ions].

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Serum concentrations of Na+, K+ and Cl- are studied, as well as the elimination of these ions in urine, in patients suffering from chronic respiratory insufficiency, being classified in two groups according to the level of hypoxemia: group A (PO2 less than 6.66 KPa) and group B (PO2 less than 8

Acute inhalation injury with evidence of diffuse bronchiolitis following chlorine gas exposure at a swimming pool.

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A previously healthy 23-year-old man with nonproductive cough and sore throat presented to the hospital a few hours after chlorine gas exposure at a fitness center swimming pool. Initial physical examination and chest radiograph were normal. Thirty-six hours later he developed worsening dyspnea and

Acute respiratory distress syndrome secondary to inhalation of chlorine gas in sheep.

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BACKGROUND Toxic industrial chemicals (TICs) are potential terrorist weapons. Several TICs, such as chlorine, act primarily on the respiratory tract, but knowledge of the pathophysiology and treatment of these injuries is inadequate. This study aims to characterize the acute respiratory distress

Chlorine inhalation-induced myocardial depression and failure.

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Victims of chlorine (Cl2) inhalation that die demonstrate significant cardiac pathology. However, a gap exists in the understanding of Cl2-induced cardiac dysfunction. This study was performed to characterize cardiac dysfunction occurring after Cl2 exposure in rats at concentrations mimicking
Acute respiratory distress syndrome is characterized by diffuse inflammatory lung injury and is classified as mild, moderate, and severe. Clinically, hypoxemia, bilateral opacities in lung images, and decreased pulmonary compliance are observed. Sepsis is one of the most prevalent causes of this

Mitigation of chlorine gas lung injury in rats by postexposure administration of sodium nitrite.

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Nitrite (NO(2)(-)) has been shown to limit injury to the heart, liver, and kidneys in various models of ischemia-reperfusion injury. Potential protective effects of systemic NO(2)(-) in limiting lung injury or enhancing repair have not been documented. We assessed the efficacy and mechanisms by

[An autopsy case of pulmonary thromboembolism associated with chlorine gas poisoning].

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We report a rare case of sudden death of a patient with acute pulmonary thromboembolism associated with chlorine gas poisoning. A 21-year-old man in a water-filtration plant accidentally inhaled highly concentrated chlorine gas. He was immediately brought to a hospital after exposure. On admission,
BACKGROUND There have been occasional reports of respiratory dysfunction associated with acute chlorine gas inhalation. However, management of acute chlorine-related inhalation injury is largely empirical, supportive, and sometimes challenging. UNASSIGNED A 43-year-old man was transferred to the

Electrophilic addition of chlorine monofluoride for PET tracers.

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OBJECTIVE We have studied the utility of [(18)F]ClF electrophilic addition to the carbon-carbon double bond of analogues of a model positron emission tomography (PET) tracer, [(18)F]EF5. The consequence of simultaneous chlorine/fluorine addition on lipophilicity and biological activity of the

Chlorine-related inhalation injury from a swimming pool disinfectant in a 9-year-old girl.

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Chlorine is a potential respiratory hazard in both occupational and household settings. The clinical sequelae of inhalation are variable in severity and timing, and subacute presentation is a concern. We report the case of a 9-year-old girl who developed dyspnea, hypoxemia, and pneumonitis

Hyperchloremic metabolic acidosis after chlorine inhalation.

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Chlorine gas inhalation is usually accompanied by pulmonary toxicity and hypoxemia; the associated acidemia, when present, has been attributed to lactic acidosis. This case report describes the development of hyperchloremic metabolic acidosis following accidental chlorine gas exposure. The mechanism

Oxygen Administration Improves Survival but Worsens Cardiopulmonary Functions in Chlorine Exposed Rats.

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Chlorine is a highly reactive gas that can cause significant injury when inhaled. Unfortunately, its use as a chemical weapon has increased in recent years. Massive chlorine inhalation can cause death within 4 hours of exposure. Survivors usually require hospitalization after massive exposure. No
A novel weakly DNA-intercalative bioreductive compound. 4-[3-(2-nitro-1-imidazolyl)-propylamino]-7-chloroquinoline hydrochloride (NLCQ-1). has been synthesized and studied as a hypoxia-selective cytotoxin in vitro. NLCQ-1, which shares a similar structure with the DNA-intercalative antimalarial drug

Multiple protective activities of neuroglobin in cultured neuronal cells exposed to hypoxia re-oxygenation injury.

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Oxidative stress is associated with the pathology of acute and chronic neurodegenerative disease. We have cloned a human neuroglobin (Nb) construct and over-expressed this protein in cultured human neuronal cells to assess whether Nb ameliorates the cellular response to experimental
This study characterizes the sequential alterations of, and relations between, multiple electrolytes in cytoplasm, mitochondria, and whole cells during hypoxia and on reoxygenation in isolated neonatal rat ventricular myocytes. Subcellular electrolyte content and distribution were measured by
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