| Acute lung injury is the common complication after severe infection, trauma and shock, etc. Its main pathological manifestation is pulmonary mesenchyma e-dema and parenchyma injury, and it is often accompanied with progressive refractory hypoxia and inflammation. Therefore, to protect the injured alveolar and to inhibit the progressive development of inflammation become the essential problem when treating All. Partial liquid ventilation using perfluorocarbon (PFC) with high oxygen and high carbon dioxide solubility can obviously raise partial pressure of blood oxygen after ALI, increase lung compliance and inhibit secretion of inflammatory factor.The main reason for hypoxia after lung injury is inadequate secretion of pulmonary surfactant ( PS) , which can cause increased surface tension of alveolar gas-liquid interface, progressive alveolar collapse, atelectasis and imbalance of ventilation perfusion ratio. So protection of physiological function of residual alveoli and increase PS secretion will improve hypoxia. The present studies show the mechanism of PLV increase pulmonary compliance and partial pressure of blood oxygen lies in the followings: 1. PFC of low tension itself is resemble surfactant and cannot be inactivated by the large amount of plasma protein after lung injury; 2. Because PFC is dense, it will gravitate to the dependent parts of the lungs primarily. The bulk of the liquid will re - open collapsed regions of lung, acting as liquid PEEP. 3. In PLV, some regions of lung, particularly the non - dependent regions, may be predominantly ventilated with gas. If pulmonary vessels in dependent lung regions are compressed by PFC in the alveoli of these regions, blood flow could be diverted towards non-dependent, aerated lung. PLV thus improves matching of ventilation to perfusion. However, thereare no reports on whether PLV can help pneumocyte type II to secrete PS or whether PLV affects the component of PS.Cascade-like inflammation caused by all kinds of infectious and noninfec-tious factors is the basis of ALI developed to ARDS. Treatment of ALI with PLV using PFC, compared with routine gas mechanical ventilation supported therapy, can inhibit intrapulmonary aggregation of neutrophil granulocyte and macropha-ges and decrease the concentration of inflammatory factor such as TNF-cuIL-lp in bronchoalveolar lavage fluid. Pathological research also proved PLV could relieve inflammatory damage of lung, but its exact mechanism is not clear yet. This project is based on the summary of latest researches, aiming at the etiology of ALI, to study the theory of treatment of ALJ using PLV. The study holds three parts: 1. The effect of partial liquid ventilation on the pulmonary surfactant in rabbit acute lung injury induced by oleic acid; 2. The effect of partial liquid ventilation on the pulmonary surfactant associated protein A in rabbit acute lung injury; 3. The effect of PFC on the activation of neutrophils NF-kB stimulated by lipopolysaccharide.Materials and MethodsParti1. Animal Preparation24 healthy New Zealand white rabbits, weighing between 2. 1 and 2. 6 kg, were were anesthetized with a 100 mg/kg of ketamine. After conventional intubation, a cuffed endotracheal tube was placed in the trachea and secured. Gas mechanical ventilation was initiated and a bolus injection of 0.4mg/kg of pancu-ronium was administered for paralysis. Mechanical ventilation was provided u-singa Siemens 900C ventilator with the following ventilatory settings: volume-controlled ventilation, tidal volume (TV) , 12 ml/kg; respiratory rate (RR) , 40 breaths/min; inspiratory to expiratory (I: E ) ratio, 1:2; the fraction of inspired oxygen (FIO2) , 1.0; and positive end-expiratory pressure ( PEEP) , 5 cm H2O. The right femoral artery was cannulated for arterial blood pressure monitoring and blood sampling. Subsequent anesthesia was maintained with an i. v. in-jectionof ketamine 20 mg kg-1 h-1. Muscle relaxation was maintained by i. v. administration of pancuroniumbromide with continuous infusionO.2...
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