Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of oxygen free radicals in the mechanism of lung damage after smoke inhalation injury was investigated. 42 dogs were used and equally divided into control and treated group. In treated group, a comprehensive anti-lipid peroxidation treatment including Ginseng-ophiopgon, hydrocortisone sodium succinate, Vit. C and E were used at 5 min, 6 hr, and 12 hr postinjury. SOD activity in blood, hypoxanthine, xanthine, uric acid, MDA and SCL in plasma, C2H6 and C2H4 in exhaled breath of dogs after smoke inhalation injury were measured. In addition, blood gas analysis and EVLW were determined to evaluate the lung damage. The results demonstrated that the injured dogs suffered from lung edema and acute lung dysfunction. MDA, SCL in plasma and C2H6, C2H4 in exhaled breath increased markedly, reaching their first peaks at 30 min. and second peaks at 24-72 hours postinjury. The values revealing in first peak in treated group were lower than that in control group. The increase of SOD activity, however, was higher in treated group than in control group. Changes of oxygen free radicals and lipid peroxidation were closely related to lung damage and respiratory dysfunction. These data showed that in early postinjury period increase of oxygen free radicals and excessive lipid peroxidation existed in lungs of dogs. And in treated group, anti-lipid peroxidation activity was increased and lipid peroxidation was inhibited. Lung damage was improved obviously. It was believed that the first peak of changes in oxygen free radicals and lipid peroxidation was related to the onset of early pulmonary damage and the stress response, and the second peak to the development of pulmonary infection and lung repaired.
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PMID:[Experimental treatment of smoke inhalation injury with anti-lipid peroxidation agents]. 228 97

Acute respiratory distress syndrome (ARDS) is characterized by sudden onset of respiratory distress, infiltrates on radiographs consistent with pulmonary oedema, hypoxaemia and increased work in breathing. Infiltrates on radiographs are bilateral, but may be patchy or diffuse and fluffy or dense. It is associated with absence of left heart failure and a PaO2/FiO2 ratio of < or =200. Ethylene vinyl alcohol copolymer dissolved in dimethyl sulfoxide (DMSO), which was approved by the US FDA in July 2005, is used as an embolic agent for cerebral arteriovenous malformation (AVM). It is a biocompatible liquid polymer that precipitates and solidifies on contact with blood, thus forming a soft and spongy embolus. We report a case of ARDS following therapeutic embolization with ethylene vinyl alcohol copolymer for cerebral AVM under general anaesthesia. Experienced perioperative physicians adopted standard anaesthetic technique and monitoring for this procedure. Acute respiratory distress and hypoxaemia developed in the patient following extubation of the trachea. Infiltrates seen on postprocedural chest radiographs were consistent with pulmonary oedema. DMSO, the solvent for the ethylene vinyl alcohol copolymer, is excreted via the lungs after administration and we postulate that DMSO was the possible cause of ARDS in this patient. Monitoring of haemodynamic parameters (invasive blood pressure, electrocardiography) and ventilatory parameters (ETCO2, SpO2, airway pressure monitoring) are important in the recognition of this possible event. One should be vigilant and anticipate this complication following therapeutic embolization with ethylene vinyl alcohol polymer for the treatment of cerebral AVM.
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PMID:Severe pulmonary oedema following therapeutic embolization with Onyx for cerebral arteriovenous malformation. 1817 30