Study On The Mechanism And Prophylaxis And Treatment Of Acute Lung Injury After Chest Explosive Trauma

Chest explosive trauma is usual in modern war. It is the emphasis and difficulty in the treatment of explosive trauma because of its complexity and high mortality. Acute lung injury(ALI), even acute respiratory distress syndrome(ARDS) after chest explosive trauma is one of main causes of mortality in wartime. The study on the mechanism and treatment of ALI after chest explosive trauma has not been reported until now. The objectives of the present study are to establish the experimental model of ALI after chest explosive trauma, and to evaluate the expression alterations of signal transduction molecules under explosive stress condition, discuss their roles in mechanisms of ALI and potential possibility for NF K B P65 and P38 MARK as therapeutic targets for ALI/ARDS; at the same time, we investigate the influence of dexamethasone and anisodamine on the pulmonary function, discuss their roles in the prophylaxis and treatment of ALI, and provide experimental basis for the treatment of ALI after chest explosive trauma. There are three parts of the study.Part One. Establishment of animal model of ALI after chest explosive trauma.The objective of this part is to establish the stable experimental animal model of ALI after explosive trauma, investigate thecharacteristics of lung injury and provide basis for further study. 64 rabbits were divided into 5 groups randomly according to the distance between denotator and animal. Group A: normal control, 8 rabbits; B: D=5cm, 12 rabbits; C: D=8cm, 12 rabbits; D: D=12cm, 16 rabbits; E:D=15cm, 12 rabbits. The rabbits were fasted before experiment for at least 6 hours, and anesthetized by 3% pentobarbital sodium intravenous injection through auricular vein. Intubations through right carotid artery and external carotid vein and ECG conducting wires were settled. We used No. 8 denotators as explosive sources and exploded them electrically. The rabbits were fastened to the experimental shelf left lying position, the denotators were fastened to the shelf , too. The axis of denotators paralleled with the intercostal spaces. Physiologic index such as respiratory rate , peripheral artery pressure and central venous pressure were recorded continuously from 5 minutes before explosion; survival time of the animal, blood gas analysis and chest X-ray examination were done at the same time points; in addition to this, rate of lung water and the contents of IL-6, IL-8 and TNF a in plasma and BALF were detected. Results: There were 36 rabbits with lung fragment wounds in the whole 64 rabbits .All the rabbits had lung blast injury of different levels. We can call group B and C, D, E seriously injured groups, moderately injured group and slightly injured group respectively. The area of lung consolidation of group B and C was above 50%, while group D, about 30%. Survival time of group D was above 24 hours except for one immediate death after trauma. It was significantly longer than that of group B and C(p<0.01). All the rabbits in group E recovered in 6 hours after trauma; The respiratory rate raised significantly in 5minutes after trauma in each group(p<0. 01). It reached the height of 87?0 per minute in 1 hour in group D, then decreased, but could not recover in 24 hours. Rabbits in group E recovered in 3 hours after trauma(p<0. 05); Rate of lung water decreased with the increase of distance between denotator and animal. RLW of group D and E decreased more significantly than that in group D(p<0. 05); X-ray examination showed that there existed patch and fused shadows early after explosion because of pulmonary hemorrhage, and it was more serious in the right lung and hilus of lung than that in the left. But in group D, the changes above mentioned had not been found until 24 hours after trauma, patch shadow was all over the lungs after 48 hours. Gradual respiratory acidosis was found in group C and D, Pa02 and Sa02 decreased sharply after trauma; on the other hand .pathological shunt and invalid ventilation was characterized by the increase of P(A-a)02. Changes of inflammatory cyt...