急性减压病大鼠肺组织粘附分子的变化

目的:探讨急性减压病大鼠肺组织中内粘附分子的改变。方法:雄性SD大鼠置于加压舱内,压缩空气在3 min内匀速加压至0.7 MPa,停留60 min后,3 min内快速减压出舱。观察减压后生存率、减压病症状。在减压后30 min、6 h、24 h取大鼠脑、肺及肝脏组织,甲醛溶液固定、切片、HE染色观测病理改变。免疫组化测定肺组织中细胞间粘附分子-1(ICAM-1)、E-选择素(E-selectin)、主要组织相容性复合体-Ⅱ(MHC-Ⅱ)的表达变化。在减压后6h、24 h前30 min,大鼠尾静脉注射2%evans blue溶液。30 min后行生理盐水灌注,收集肺组织,观测肺组织蓝染程度,酶标仪测定血浆中evans blue含量。结果:肺、肝及脑组织在减压后30 min出现水肿、淤血等病理表现。和正常组比较,肺组织中ICAM-1、E-selectin、MHC-Ⅱ在减压后明显上升,并呈现动态变化。相对于正常组,减压后6 h、24h肺组织血浆中evans blue含量明显增加。结论:气泡导致的,粘附分子介导的血管内皮受损是减压病的发病机制之一。

Change of adhesion molecules in the lungs of rat with decompression sickness

Objective: To investigate the change of adhesion molecules in the lungs of rats suffered with decompression sickness(DCS).Methods: Male SD rats were placed in the hyperbaric chamber,the chamber was compressed within 3 minutes to depths of 7 absolute atmosphere(ATA) and held at the designated depth for 60 min,then rapidly decompressed(3 min) to the surface.Rats were observed for signs of DCS after decompression.The brains,hepatics,and lungs were removed at 30 min,6 h,24 h post decompression,fixed and stained with hematoxylin eosin for routine histologic analysis.Lung paraffin sections were immunostained for the expression of intercellular adhesion molecule-1(ICAM-1),E-selectin and major histocompatibility complex class II molecule(MHC-II).2% evans blue dye in normal saline was injected 30 minutes prior to 6 h,24 h before decompression.After 30 min,animals were perfused with 0.9% normal saline and lungs were harvested.Evans blue in the plasma was quantified by wavelength spectrophotometric analysis at 620 nm.Results: Results showed that there were hemorrhage and edema changes in the lungs,liver and brain at 30 min post decompression.Compared with control animals maintained at 1 ATA,the levels of E-selectin,ICAM-1 and MHC-II in the lungs of DCS rats were significantly increased post decompression.Compared with control animals,evans blue in the plasma was much higher at 6 h,24 h post decompression.Conclusion: The bubble-induced adhesion molecule-mediated endothelial activation may be involved in the pathogenesis of DCS.