首页> 外文期刊>European journal of applied physiology >Treatment of micro air bubbles in rat adipose tissue at 25 kPa altitude exposures with perfluorocarbon emulsions and nitric oxide
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Treatment of micro air bubbles in rat adipose tissue at 25 kPa altitude exposures with perfluorocarbon emulsions and nitric oxide

机译:用全氟化碳乳剂和一氧化氮处理在25 kPa高度暴露于大鼠脂肪组织中的微气泡

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Introduction: Perfluorocarbon emulsions (PFC) and nitric oxide (NO) releasing agents have on experimental basis demonstrated therapeutic properties in treating and preventing the formation of venous gas embolism as well as increased survival rate during decompression sickness from diving. The effect is ascribed to an increased solubility and transport capacity of respiratory gases in the PFC emulsion and possibly enhanced nitrogen washout through NO-increased blood flow rate and/or the removal of endothelial micro bubble nuclei precursors. Previous reports have shown that metabolic gases (i.e., oxygen in particular) and water vapor contribute to bubble growth and stabilization during altitude exposures. Accordingly, we hypothesize that the administration of PFC and NO donors upon hypobaric pressure exposures either (1) enhance the bubble disappearance rate through faster desaturation of nitrogen, or in contrast (2) promote bubble growth and stabilization through an increased oxygen supply. Methods: In anesthetized rats, micro air bubbles (containing 79 % nitrogen) of 4-500 nl were injected into exposed abdominal adipose tissue. Rats were decompressed in 36 min to 25 kPa (~10,376 m above sea level) and bubbles studied for 210 min during continued oxygen breathing (FIO2 = 1). Rats were administered PFC, NO, or combined PFC and NO. Results: In all groups, most bubbles grew transiently, followed by a stabilization phase. There were no differences in the overall bubble growth or decay between groups or when compared with previous data during oxygen breathing alone at 25 kPa. Conclusion: During extreme altitude exposures, the contribution of metabolic gases to bubble growth compromises the therapeutic effects of PFC and NO, but PFC and NO do not induce additional bubble growth.
机译:简介:全氟化碳乳剂(PFC)和一氧化氮(NO)脱模剂在实验基础上已显示出可治疗和预防静脉气体栓塞的形成的治疗特性,并提高了潜水减压病的生存率。该作用归因于呼吸气体在PFC乳剂中的溶解度和传输能力增加,并且可能通过NO升高的血流速度和/或去除了内皮微泡核前体而增强了氮的清除。先前的报告表明,在海拔高度暴露期间,代谢气体(特别是氧气)和水蒸气有助于气泡的生长和稳定。因此,我们假设在低压下暴露时施用PFC和NO供体或者(1)通过更快地脱氮来提高气泡消失率,或者相反(2)通过增加氧气供应来促进气泡生长和稳定。方法:在麻醉的大鼠中,将4-500 nl的微气泡(含79%的氮)注入暴露的腹部脂肪组织中。在36分钟内将大鼠减压至25 kPa(比海平面高10376 m),并在持续的氧气呼吸(FIO2 = 1)期间研究了210分钟的气泡。给大鼠施用PFC,NO或联合使用PFC和NO。结果:在所有组中,大多数气泡都是短暂增长的,随后是稳定阶段。各组之间的总气泡增长或衰减没有差异,或者与之前在25 kPa氧气呼吸期间的数据相比,没有任何差异。结论:在极端高度暴露期间,代谢气体对气泡生长的贡献会损害PFC和NO的治疗效果,但PFC和NO不会诱导额外的气泡生长。

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