CAJ | 학술논문

目的探讨烟雾吸入后肺泡内表而活性物质(PS)亚型分布的变化和可能机制,以及其与PS活性抑制的关系.方法采用大鼠烟雾吸入伤模型,分别检测了正常对照组及致伤2、6、12、24 h大鼠的动脉血气、肺水量、支气管肺泡灌洗液(BALF)表面张力特性、BALF总磷脂(TPL)、总蛋白(TP)、白蛋白(Alb)含昔及α1抗胰蛋白酶(α1-AT)活性、肺泡腔内PS亚型超微结构.结果大鼠烟雾吸入伤后出现急性呼吸衰竭和严重肺水肿;BALF最小表面张力(STmin)进行性升高;BALF中TPL、TP、Alb及α1-AT增加,且STmin与α1-AT/TP、α1-AT/Alb比值的变化相关显著;伤后早期肺泡腔内PS板层体和囊泡聚集,管髓体破坏;后期大量囊泡聚集,板层体少,管髓体几乎缺失.结论烟雾吸入伤后肺泡腔内PS亚型分布及转化异常是引起PS活性抑制的主要原因之一,α1-AT与血浆蛋白比例失衡可能起重要作用.
목적 탐토연무흡입후폐포내표이활성물질(PS)아형분포적변화화가능궤제,이급기여PS활성억제적관계.방법 채용대서연무흡입상모형,분별검측료정상대조조급치상2、6、12、24 h대서적동맥혈기、폐수량、지기관폐포관세액(BALF)표면장력특성、BALF총린지(TPL)、총단백(TP)、백단백(Alb)함석급α1항이단백매(α1-AT)활성、폐포강내PS아형초미결구.결과 대서연무흡입상후출현급성호흡쇠갈화엄중폐수종;BALF최소표면장력(STmin)진행성승고;BALF중TPL、TP、Alb급α1-AT증가,차STmin여α1-AT/TP、α1-AT/Alb비치적변화상관현저;상후조기폐포강내PS판층체화낭포취집,관수체파배;후기대량낭포취집,판층체소,관수체궤호결실.결론 연무흡입상후폐포강내PS아형분포급전화이상시인기PS활성억제적주요원인지일,α1-AT여혈장단백비례실형가능기중요작용.
Objective To explore changes in the distribution of pulmonary surfactant (PS)subtypes in alveolar spaces and the possible mechanisms involved, and also to investigate the relationship between changes and the inhibition of PS activity after smoke inhalation. Methods Following induction of smoke inhalation injury in rats, arterial blood gas levels, lung water volume, surface tension of bronchoalveolar lavage fluid ( BALF), contents of total phospholipids ( TPL), total proteins ( TP), albumin ( alb), and activity of α1-antitrypsin (α1-AT) in BALF, the uhrastructures of PS subtypes in alveolar spaces were determined respectively in normal control and injured animals at 2 h, 6 h, 12 h and 24 h after injury. Results After smoke inhalation, the animals displayed acute respiratory failure and serious pulmonary edema, progressive elevation of minimum surface tension (Stmin) in BALF, marked increase in the levels of TPL, TP, Alb, and α1-AT in BALF., and significant correlation between changes in Stmin and α1-AT/TP ratio, as well as in α1-AT/Alb ratio. In the early stage after injury, lamellar bodies and vesicles aggregated in alveolar spaces with destruction of tubular myelins, while a great many vesicles and a few lamellar bodies aggregated, with obvious deficiency in tubular myelins in the late stage. Conclusions Changes in the distribution and abnormal conversion of PS subtypes in alveolar spaces are one of the important causes for the inhibition of PS activity after smoke inhalation, and the imbalance of α1-AT/plasma proteins ratio may play an important role in it.