模拟大深度快速上浮脱险兔血浆血管性血友病因子和一氧化氮水平变化

Experimental Study on the Changes of vWF and NO in Rabbits with Decompression Injury induced by Simulated Deep Fast Buoyancy Ascent Escape

目的:研究大深度快速上浮脱险兔血浆血管性血友病因子(vWF)和一氧化氮(NO)浓度变化及在减压损伤中的意义。方法:成年雄性新西兰兔16只,以2t/4指数速率加压至1.5MPa(表压),稳压停留80s,以30kPa/s匀速减压至常压。出舱后观察动物行为并统计减压病发病率。实验前及出舱后各采血2ml,4℃离心分离血浆,分别采用酶联免疫吸附法及硝酸还原酶法检测实验兔血浆vWF和NO浓度。结果:实验兔减压病发病率68.75%(11/16);实验后兔血浆vWF和NO浓度分别为3.59±0.31μg/L和117.00±36.00μmol/L,较实验前(2.65±0.26μg/L和64.50±26.60μmol/L)显著升高,差异有统计学意义(P<0.01)。结论:血浆vWF、NO浓度升高可以作为大深度快速上浮脱险机体减压性内皮损伤的监测指标和减压病发病的可能机制之一。

Objective：To investigate the changes of von Willebrand Factor（vWF）and Nitric oxide（NO）in rabbits with decompression injury induced by simulated deep fast buoyancy ascent escape and to evaluate their role in the pathogenesis of decompression sickness.Method：Sixteen male SD rabbits were compressed to a pressure of 1.5 MPa at an exponential rate of 2 t/4 with compressed air,after staying for 80s at the above pressure,the animals were decompressed to atmospheric pressure at linear speed （30KPa/s）.Morbidity and symptoms of decompression sick-ness in animal model was monitored.The blood samples were collected before compression and after decompression respectively.vWF and NO were measured immediately.Results：The Morbidity of decompression sickness in animal model was 68.8%.Compared with those before compression,vWF levels[（2.65 ± 0.26 ）μg/L]and NO levels[ （64.5 ± 26.6）μmol/L]in the of rabbits were increased significantly after decompression [（3.59 ± 0.31 ）μg/L, （1 1 7.0±36.0）μmol/L]（P 〈0.01）.Conclusion：The changes of vWF and NO in the could be used as indicators for the occurrence of decompression injury induced by simulated deep fast buoyancy ascent escape.