| Objective: Acute Lung Injury is a inflammatory reaction which is out of control. These factors of severe infection, trauma, shock lead to pulmonary edema and Unexpanded lung. It's pathologic character is extensive injury of blood capillary endothelial cell and alveolar epithelium cell. The clinical situation is respiratory distress and intractable hypoxemia. The pathogenesis is very complicated. There are many effector cells and cytokines to participate in this disease. Now many investigator suggest that the alveolus mononuclear and polymorphonuclear leukocyte produce the complement C5a, TNF-α, IL-β, which can start the response of inflammation cascade. They also stimulate the cells in lung to produce chemotactic factors such as ICAM-1, the ICAM-1 mediates the inflammatory cells migrate into the interstitial tissue of lung and alveolus, Above all the polymorphonuclear leukocyte (PMN) will be activation, which lead to the respiratory burst and release masses of cytokines and mediators. The balance of promote inflammatory/ anti-inflammatory cytokines system in body is destruction. The condition is difficult to control. It developed ARDS ultimately. In this study ,the rat was injected oleic acid to make an animal model of acute lung injury. We measure the pulmonary coefficient (PC) and the lung permea- bility index (LPI), the oxidative stress and the expression of chemotactic factor and inflammation factor in lung tissue. In order to search the medicine to protect acute lung injury. We infused ulinastatin (UTI) to the rat and analysis the alteration of above index. To explore the the prevention and therapeatic effect of UTI on acute lung injury in rat and probable mechanisms.Methods: The animal modle of acute lung was established by injecting oleic acid into the superior vena of rat. After injection of oleic acid the oral lip of rat appears cyanosis. Their frequency of respiratory turns very high. Forty healthy wistar rat of either sex weighting 250g were randomly divided into four groups: control group, oleic acid injury group, UTI prevent group, UTI treat group. After four hours, the level of PC,LPI, MDA,SOD, MPO was measured, and the expression of ICAM-1, TNF-α, IL-β in lung tissue was examined by immunochemistry, meanwhile the histopathological change of lung tissle was observed. Then we infused UTI to the rat and examined the above items.Results:1 Change of pathological section: There was no alteration in lung tissue in control group. In injury group severe congestion and lung edema and the lung swelled. In UTI prevent group and UTI treat group there were slight alteration compared with that in injury group.Light microscope(HE): The injury group can be observed Local hemorrhage the focal infarct form; The edema of alveolue Many inflammatory cell infiltration. Electron microscope The I form alveolar epithelium swelled obviously some part of karyolemma nerniated outside and heterochromatin aggregated lightly under karyolemma, the electron-density of cytoplasm reduced and vacuolar degeneration could be seen in mitochondria and rough endopasmicreticulum expanded into cystis. 1.2.2 TheⅡform alveolar epithelium: The microvillus shedding and confluence partly majority of lamellar body developed a big vacuoles by evacuating. organella reduced in cytoplasm and the arrangement of rough endopasmicreticalum was irregular. 1.2.3 Vascular endothelial: Organcells reduced and the eletron-density of cytoplasm increased, thickness of intima was irregular and basilar membrane under endotheliocyte was vague. 2 Changes of pulmonary coefficient: The numeric value of pulmonary coefficient in control group was 0.006±0.001, in injury group was 0.011±0.004 (p<0.01 vs control group), in UTI prevent group was 0.008±0.002 (p<0.01vs injury group), in UTI treat group was 0.010±0.003 (p<0.05 vs injury group). 3 Changes of lung permeability index: The numeric value of lung permeability index in control group was 0.028±0.007, in injury group was 0.345±0.053 (p<0.01 vs control group), in UTI preven...
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