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An unusual trichloroethanol fatality attributed to sniffing trichloroethylene.
J Anal Toxicol
March 2008
Office of the Chief Medical Examiner, 7007 - 116 Street NW, Edmonton, Alberta, Canada T6H 5R8.
We report the death of a 28-year-old man due to sniffing a contact cement containing trichloroethylene. Initial testing revealed the presence of 80 mg/L trichloroethanol in cardiac blood, and the death was ruled as being due to trichloroethanol toxicity resulting from chloral hydrate ingestion. However, further investigation of the case revealed that the trichloroethanol resulted from trichloroethylene abuse.
View Article and Find Full Text PDFDrug-induced pulmonary edema and acute respiratory distress syndrome.
Clin Chest Med
March 2004
Section of Pulmonary Medicine, Department of Medicine, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.
Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia.
View Article and Find Full Text PDFLoxapine intoxication: case report and literature review.
J Anal Toxicol
October 2000
The Office of the Cuyahoga County Coroner, Cleveland, Ohio 44106, USA.
Loxapine is a dibenzoxazepine tricyclic compound used to treat schizophrenia in the United States since 1976. Metabolism includes demethylation to its primary metabolite, amoxapine. There are few documented reports of the disposition of loxapine in deaths due to overdose.
View Article and Find Full Text PDFInhibition of cytochrome P-450 attenuates hypoxemia of acute lung injury in dogs.
Am J Physiol
April 1996
Department of Pharmacological and Physiological Science, Saint Louis University, School of Medicine, Missouri 63104, USA.
The intravenous administration of ethchlorvynol (ECV), in dogs, resulted in an acute lung injury (ALI) characterized by a 200 +/- 80% increase in venous admixture and a 142 +/- 30% increase in extravascular lung water (EVLW). Pretreatment with the cytochrome P-450 inhibitor 8-methoxypsoralen prevented the ECV-induced increase in venous admixture but not the increased EVLW. These findings parallel those reported for cyclooxygenase inhibition in ECV-induced ALI and suggest that an arachidonic acid (AA) metabolite of pulmonary cytochrome P-450 activity may mediate the increase in venous admixture of ALI.
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