【作者】 梁海龙；

【导师】 江朝光；

【作者基本信息】 中国人民解放军军医进修学院 ， 心血管外科， 2004， 硕士

【摘要】 全氟异丁烯(Perfluoroisobutylene，PFIB)是一种低分子氟碳化合物，常温下气态，无色并近于无味。其有极强的呼吸道毒性，属光气类毒气，而毒性达到光气的十倍，吸入后可致严重肺损伤。PFIB是聚氟工业常见的副产物，含氟塑料Teflon加热至300℃以上亦可产生。由于Teflon有化学性质稳定、摩擦系数小、绝缘、耐热等优点，被广泛用于民间各个方面，屡有报道在火灾事故中发生人吸入PFIB中毒事件。鉴于PFIB来源广、毒性大，已成为威胁人民健康和公共环境卫生的隐患。此外，PFIB还能穿透普通防毒面具的滤毒罐，难以防护，被各国有关部门认为是潜在的军用毒剂和恐怖攻击手段。因此，研究PFIB的毒性作用特点，探索有效的防护、治疗方法，于军于民都有着迫切的现实意义。 目前对PFIB的毒理机制未完全搞清，因此缺乏针对性的防军医进修学院硕士毕业论文中文摘要护、治疗措施。我们从临床医学的角度出发，首次选用大动物(杂种犬)进行PFIB染毒，完成了以下工作: 1.通过改造建立犬PFIB染毒系统，保证其吸入浓度稳定均一(p>0.05)的pFIB。经摸索确定吸入0.30一o.32mg/L的PFIB3omin后，实验犬在22h内PaOZ压10:均降至ARDS水平。考察了犬吸入PFIB后临床表现、肺及其他脏器的病理改变。认为所造成肺损伤属严重的ARDS。 2.检测了犬吸入PFIB前后循环TNF一a、IL一6、IL一8变化。发现其中IL一8水平持续显著升高(p<0 .05)，而，I’NF一a、IL一6无明显变化印>.05)，认为严重肺损伤很可能是潜伏期肺内大量PMN扣押、激活后造成。 3.对所建立ARDS模型进行动脉一静脉无泵型ECMO治疗的研究:作为对照，呼吸机辅助能提高犬模型SaO2，但随着肺实变加重，逐渐难以保障基本氧需求;ECMO组，对ARDS模型先行呼吸机辅助，当无法维持sao:在90%以上，立即开始颈动脉一颈静脉无泵ECMO由于犬肺气体交换面积明显减小，而所用膜肺表面积有限(lmZ)，所行ECMO难以达到完全氧合。但与呼吸机辅助协同氧合，可维持SaO:在90%以上，第4公乏军医进修学院硕圣毕业论文中文摘要paCO:在20一3ommHg。此外，A一v无泵EeMo可显著降低模型队P(p<0.05)，从而改善右心功能。转流40h结束，处死取肺病检，肺损伤变化改善。更多还原

【Abstract】 Perfluoroisobutelene(PFIB) is a kind of low-molecular-weight fluorocarbon compound, which exists as colorless gas with almost no smell at normal tempetature. PFIB is of the same kind of toxic gas as phosgene, but ten times as toxic as phosgene, and inhalation of PFIB can induce severe lung injury . PFIB can be generated as a commom byproduct in fluoropolymer industry, and also by pyrolysis of Teflon with temperature above 300 C . As Teflon is of many benifitial properties, it is widely used in people life, so poisoning cases by inhalation of PFIB often happen during fire accidents .Up to now, the specific mechamisms of PFIB’ s toxic funtion has not been thoroughly interpreted, correspondingly we can take little anti-measures to protect and treat. From view of clinical medicine, we for the 1st time chose big animal(mongrel) as poisoned object, several work has been finished as follows:1. Constructed inhalation system fit for mongrel to ensure that concentration of PFIB during inhalation by mongrel kept stable and constant (p>0.05)o We established that PaO2/FiO2 of mongrel invariably reached level ofARDS 22 hours after inhalation of PFIB with concentration of 0.30-0.32mg/L for 30 minutes, and by observation of clinical signs and pathologicchanges we concluded that inhalation of PFIB induced severe ARDS.2. We measured levels of TNF-a, IL-6, IL-8 in mongrel blood circulation before and after inhalation of PFIB, and found level of IL-8 elevated significantly after inhalation, whereas the other two cytokines did not change significantly. Thereby we speculated that lung injury after inhalation of PFIB may be result of PMN recruitment and activation in lung during latency.3. We studied therapeutic effect of artery-vein pumpless ECMO: as control, assist by ventilator is capable of increase mongrel’ s SaO2, but as the lung gradually became solid, basic oxygen intake of mongrel could hardly be provided by ventilator; as for ECMO group, we began ventilator assist on ARDS model first. As soon as it can not keep SaO2 above 90%, we start A-V pumpless ECMO using jugular vessels,, As lung area capable of air exchange reduced significantly and area of the oxygenator used is also limited, the ECMO is not capable of complete oxygenation by itself . When combined with mechanical ventilation, SaO2 kept above 90%, and PaCO2 kept between 20 and 30mmHg. Moreover A-V pumpless ECMO is capable of reducing model ’ s PAP ( p<0.05 ) , thereby improve right ventricular function. After 40 hours ECMO were ended, and pathologic examination of lung show signs of improvement.更多还原