| Acute lung injury (ALI) is an acute progressive ischemic respiratory failure induced by various reasons except cardiogenic factors, and its serious stage is acute respiratory distress syndrome (ARDS). ALI is caused by excessive inflammation reaction, numerous effective cells (such as macrophage, neutrophil, etc.) and inflammatory media take part in this reaction. During process of ALI, inflammatory factors (such as TNF- a , IL-1 and IL-8) increase. Inflammatory cytokines could induce other inflammatory media in cascade way, these media can increase pulmonary capillary permeability, cause interstitial edema and neutrophil exudation. The principle for ALI treatment is managing original causes and effective oxygentherapy. But oxygentherapy via respiratory canal has no resultful effects on severe ALI character with handicap of pulmonary capillary permeability, which results in high mortality. In this study, by means of oxygen carrying by solution, we investigate the effects of hyperroxia solution administered intravenously or orally on ALI induced by oleic acid and underlying mechanism and bring forward new measures for patients undergoing anoxemia resulted from various reasons.PART ONEOBJECTIVE: To investigate the effects of hyperoxia solution (HO) administered intravenously on ALI in rabbits induced by oleic acid. METHODS: HO was prepared from Ringer's solution. 24 rabbits were randomly divided into four groups with 6 in each group : control group (group C), oleic acid group (group A), treatment group B1 and group B2. ALI model was established in group A and group B by giving oleic acid 0.06 mL kg-1 , while in group C salt liquid was given. Ringer's liquid was administered iv in group A and C, 10 mL kg-1 or 20 mL kg-1 HO was administered iv in group B1 or B2 30mins after the oleic acid infusion. MAP PaO2 PaCO2 were measured. Two hours later the animals were killed and myeloperoxidase (MPO), content of lung water, lung/body ratio were measured. TNF-a and IL-8 in plasm and BALF were measured. Pathologic changes of lungs were observed under microscope. RESULTS: Comparing with group C, the PaO2 decreased significantly while MPO, content of lung and lung/body ratio significantly increased in group A (P<0.01). Local hemorrhage, interstitial edema, alveoli exudation and inflammatory cells were observed in lungs in group A. In group B2, PaO2 significantly increased (P<0.05) after HO infusion. MPO and lung water content decreased (P<0.01). Only mild pathological changes were observed in group B. CONCLUSION: HO administered intravenously has therapeutic effects on ALI induced by oleic acid.PART TWOOBJECTIVE: To investigate the effects of HO administered orally on ALI induced by oleic acid. METHOD: 18 rabbits were randomly divided into three groups with 6 in each group: oleic acidgroup (group A), treatment group (group T) and prevention group (group P). ALI model was established by giving oleic acid 0.06 mL kg-1, 20 mL kg-1 Ringer's liquid was administered orally in group A; 20 mL kg-1 HO was administered orally after iv oleic acid in group T and 20 mL kg-1 HO was administered orally before iv oleic acid in group P. RESULTS: The MAP, PaO2 decreased significantly in group A and T. Alveolar interval thickened significantly and bleeding and plentiful exudation was observed under microscope. Comparing with group A, in group P, MAP, PaO2 significantly increased(P<0.01). Thickened alveolar interval relief and little exudation were observed. CONCLUSION: HO administered orally can prevent ALI in rabbits induced by oleic acid.
|
PDF Full Text Request