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雾化二甲基亚砜治疗烟雾诱导的肺损伤。

Treatment of smoke-induced pulmonary injury with nebulized dimethylsulfoxide.

作者信息

Kimura R, Traber L D, Herndon D N, Neuhaus G D, Traber D L

机构信息

Department of Anesthesiology, University of Texas Medical Branch, Galveston.

出版信息

Circ Shock. 1988 Aug;25(4):333-41.

PMID:2458858
Abstract

Inhalation injury was produced in sheep that were chronically prepared for study. The injury was induced by insufflating them with smoke from burning cotton cloth. One group of animals was treated with the oxygen-free radical scavenger dimethylsulfoxide (DMSO) and heparin. Another group received heparin treatment alone, and a third was untreated. The drugs were nebulized into the tracheostomy at 4-hr intervals beginning 1 hr after injury. Following the inhalation injury, lung lymph flow and extravascular lung water measured by thermal-dye dilution technique were both increased. These elevations were associated with minor increases in pulmonary artery pressure, and, thus, since the lymph to plasma protein ratio was unchanged, this increased extravascular fluid formation was probably the result of an elevated microvascular permeability. These changes were associated with a reduction in alpha 2 macroglobulin antiprotease activity. The treated groups showed much smaller responses to the inhalation insult. This was especially true in the animals that received the DMSO. These findings support the concept that oxygen free radicals are responsible for the pulmonary edema associated with inhalation injury.

摘要

在为研究而长期准备的绵羊身上造成吸入性损伤。通过向它们吹入燃烧棉布产生的烟雾来诱导损伤。一组动物用无氧自由基清除剂二甲亚砜(DMSO)和肝素治疗。另一组仅接受肝素治疗,第三组未治疗。在损伤后1小时开始,每隔4小时将药物雾化到气管造口处。吸入性损伤后,通过热染料稀释技术测量的肺淋巴流量和血管外肺水均增加。这些升高与肺动脉压的轻微升高有关,因此,由于淋巴与血浆蛋白的比率未变,这种血管外液体积聚增加可能是微血管通透性升高的结果。这些变化与α2巨球蛋白抗蛋白酶活性降低有关。治疗组对吸入性损伤的反应要小得多。接受DMSO治疗的动物尤其如此。这些发现支持了氧自由基是吸入性损伤相关肺水肿的病因这一观点。

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