Establishment Of Simple Blast Lung Injury Model With Rabbits And The Research Of The Early Relevant Treatment After Injury

ObjectiveEarly chest blast injury research focused on injuries about the multi-factorof fragments composited shock waves, and the main death causes werehemorrhagic shock and acute respiratory failure,which the pathogenicmechanism is more complex.But for pure BLI, the pathogenesis of respiratoryfailure which was Caused by the shock wave is the relative lack of.Through theestablishment of a rabbit with mild and moderate to severe pure BLI model byhigh-energy shock wave,and instillment of the pulmonary surfactant into airwayfor treatment after injury,the early pathological physiology, pathology andrelated indexes were observed after injury for exploring the occurrence anddevelopment of primary acute lung injury which caused by the explosion.It canprovide a new theoretical basis for the further strengthening of the chest blastinjury early comprehensive treatment.Methods1．35New Zealand rabbits were randomly divided into three groups:thenormal control group(A),the moderate injury group(B) and the mild injurygroups(C).After intramuscular anesthesia, the head,abdomen and limbs of therabbits were covered with thicker pad to prevent brain and limbs blastinjury.Then,placed in blasting test bench,8#paper electrical detonators wasthe site of the explosion source for static bursting.After injury,toxic gases whichwere produced by the explosion were rapidly discharge of,and rabbits were given to the corresponding appropriate treatment.And then each group basicvital signs,arterial blood gases,TNF-α,IL-6,pleural effusion,lung water contentand other relative indicators were dynamic monitored.Bronchoalveolar lavagewas to collect lavage fluid for detection of concentration and activity of thepulmonary surfactant.The lung tissue had been conducted to routinepathological examination.Observed for three days,the rabbit mortality wasrecorded.2．26New Zealand rabbits which were successfully established into thesevere pure blast lung injury model were randomly divided into two groups:thetreatment group(A) and the untreatment group(B).The treatment group wereinstilled pulmonary surfactant into airway for treatment after injury.But theuntreatment group did not give pulmonary surfactant.Then,compared with theuntreatment group,efficacy were observed by blood gas analysis, lung watercontent and so on.Result1．Basic vital signs: After injury,rabbits were emerged short,shallow andrapid breath,and the lips gradually cyanosis.The8rabbits of group Bimmediately performed apnea which was continued about30s to120s.As theobservation time,breath gradually decresed and smoothed after injury2h～3h.But the respiratory frequency of group A and B were higher than group Cwithin24h.Comparing with group A,blood pressure of group B and Csignificantly reduced in10min after injury, and there were significant differences（P <0.05）.However, when the blood pressure of group B and C graduallyrecovered,it also was lower than group A in6h after injury（P <0.05）.2．Arterial blood gases,TNF-α and IL-6:Comparing with group A,PaO2ofgroup B and C significantly increased in30min after injury（P <0.05）,andreached the maximum which had significant discrepancy between group B andC at1h after injury（P <0.05）.Then,it which was higher than group A was gradually reduced（P <0.05）,and maintained at normal level at2h～6h afterinjury（P>0.05）.At last,PaO2of group B and C,respectively at12h and24h afterinjury,was significantly lower than group A,and the difference had statisticallysignificant（P <0.05）.PaCO2of group B and C gradually decreased afterinjury,and respectively started to decrease significantly at2h and6h afterinjury(P <0.05),and reached the minimun at6h and12h afterinjury,respectively(P <0.05).P(A-a)O2was calculated according tocorresponding PaO2and PaCO2.P(A-a)O2of group B and C which were lowerthan group A at1h after injury(P <0.05) started to be higher than group A at6hand12h after injury,respectively(P <0.05).Then it continued at a higher level.BEof group B gradually started to decrease,and significantly reduced at6h afterinjury(P <0.05).The group C had significantly reduced at24h after injury(P<0.05).HCO3-of group B and C also showed a decreasing trend after injury,andwere significantly lower than group A at12h and24h after injury,respectively(P<0.05).Comparing with group A,TNF-α and IL-6of group B and C hadsignificantly increased after injury（P <0.05）.3．The changes of pulmonary surfactant in bronchial alveolar lavagefluid:Not only both TPL and TP of group B and C were obviously higher thangroup A after blast lung injury（P <0.05）,but also the DSPC of group B and Cwere more higher than group A also（P <0.05）.Although,the results showed thatthe group B and C of the ratio of DSPC/TPL and DSPC/TP had no difference（P>0.05）,they were higher than group A（P <0.05）.4`．Pleural effusion,lung water content,mortality and lung histopathologicalchanges:Lung water content of group B and C were significant higher thangroup A（P <0.05）.Compared with group A,both group B and C had performedvarying degrees of unilateral or bilateral pleural effusion which was dark red orpink color,but the content of pleural effusion of group B were more than group C（P <0.05）.The Main lung pathology:diffuse sheet congestion were ranged from pulmonary surface,and a large number of dark red foam was overflow at thelung section.The alveolar cavities were filled with diffused hemorrhage andexudate which was filled with a large number of white blood cells undermicroscope.The alveolar cavities were varied degrees fusion or liked“pulmonary bullae” change.Becaues of the rapture of the alveolar walls,thecapillary bed in the alveolar was decreased.Pneumonedema also was observedin interstitial lung.The closer injury distance,the more severe degree ofinjury.With diminution of the injury distance, the group B mortality(53.85％) wasmore higher than the group C(30.77％).5．Treatment of blast lung injury:When rabbits which were severepulmonary blast injury were instilled with pulmonary surfactant into airway,therabbits PaO2was significantly increased(P <0.05),compared with the controlgroup.But the survival time between the two groups had no significantdifference(P>0.05).Conclusion1．Model of group B can better simulate the characteristics of simple blastlung injury. Because of apparent lung injury,the relatively stable condition,andthe relatively long survival time, good reproducibility can be used as the idealblast lung injury model.2．After mild and moderate blast lung injury,the early arterial blood gas orthe pulmonary gas exchange which did not apparently decrease was prone toconceal or mislead pathogenetic condition.3．When the pulmonary surfactant of content and activity increased at initialstage of blast lung injury,it played an important role in maintaining respiratoryfuction stable in a period time after injury.4．It was the major cause of early death that acute respiratory failure whichwas developed into in a short time,because progressive exacerbation of theasymmetrical pneumorrhagia and the alveolar and interstitial pneumonedema,which notably maked the function of pulmonary gas exchangedegrade.5．Although pulmonary surfactant had a certain improvement in lungventilation dysfunction after severe blast lung injury,there was no significantimprovement in the survival time.