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Objective To explore the role of strategy of conservative fluid management combining with lung-protective ventilation in treating acute lung injury. Methods 40 cases with final diagnosis of acute lung injury were selected and randomly divided into experimental group(22cases) and control group(18cases). Between two groups,on the basis of lung-protective ventilation,therapy policy of conservative fluid management was carried out in experimental group, and strategy with a liberal fluid management was taken in the other group. Hie duration of mechanical ventilation and intensive care together with the incidence rate of nonpulmonary complications( congestive heart failure,renal failure and liver failure) were compared between both groups. Results When compared with the control group,the experimental group had the shorter duration of mechanical ventilation and intensive care( P < 0.05 ). And the incidence rate of nonpulmonary complications were similar in both groups. Conclusion Strategy of conservative fluid management combining with lung-protective ventilation could shortened the duration of mechanical ventilation and intensive care for patients with acute lung injury without increasing the incidence rate of nonpulmonary complications, which was an effective and safe treatment and deserved consulting in clinical work.
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Objective To evaluate clinical the effects and significance of the occurence and development of varies intervention on control of acute lung injury(ALI)in clinical practice.Methods Sixty-nine ALI patients were randomly divided into three groups:traditional ventilation therapy group(n=17),low dose ulinastatin intervention with traditional ventilation therapy group(n=24)and high dose ulinastatin intervention in lung protective ventilation therapy group(n=28).We compared the changes of pneumodynamics,arterial blood gas and hemodynamics among these groups.Resident time in ICU,time course of mechanical ventilation and mortality of these groups were also compared.Results Large dose ulinastatin intervention in lung protective ventilation therapy group had further improved influence on pneumodynamics,arterial blood gas and puhnonary oxygenation than other groups(P＜0.05)and no mechanical ventilation induced lung injury was found in the group.There were no obvious differences in pneumodynamics,arterial blood gas and pulmonary oxygenation between the other two groups(P＞0.05).Lung injuries induced by mechanical ventilation were all observed in these two groups.There were no obvious differences in hemodynamics among the three groups(P＞0.05).Conclusions Large dose ulinastatin intervention in lung protective ventilation can improve pneumodynamics,arterial blood gas and pulmonary oxygenation of ALI patients.It could decrease the incidence of ventilator induced lung injury(VILI).The treatment should been applied prospectively in clinical practice.
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Objective To investigate the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in the lung tissue in a rat model of ventilator-induced lung injury. Methods Thirty healthy male SD rats weighing 200-250g were randomly divided into 3 groups( n = 10 each) : group A spontaneous breathing; group B small tidal volume (VT = 7 ml?kg-1, RR = 40 bpm, FiO2=0.21) and group C large tidal volume (VT = 40 ml?kg-1, RR = 20 bpm, FiO2=0.21). The animals were mechanically ventilated for 4 h in group B and C. The lung injury was assessed by measurement of PaO2 /FiO2 . At the end of the experiment the animals were killed and the lungs were removed. The right lung was used for determination of the expression of mRNAs of MMP-2, MMP-9, TIMP-1 and TTMP-2 using RT-PCR and histologic examination. The left lung was weighed and then lavaged. The broncho-alveolar lavage fluid (BALF) was collected for total WBC and neutrophil counts and determination of total protein content and gelatinase activity. After lavage the left lung was heated at 60℃. The W/D lung weight ratio was calculated. Results PaO2/FiO2 was significantly lower after 4h mechanical ventilation in group C than in group A and B. The total WBC count and total protein content in BALF were significantly higher in group C than in group A and B. The W/D ratio of the left lung was significantly higher in group C than in group A and B. Microscopic examination showed that there were marked WBC infiltration and destructive changes of alveolar walls in group C. The levels of gelatinase (MMP-2 and MMP-9) activities in BALF were significantly higher in group C than in group A and B. The expression of the mRNA of MMP-2 and MMP-9 was significantly higher in group C than in group A and B, but there was no significant difference in the expression of the mRNA of TIMP-1 and TIMP-2 between group C and group A and B. Conclusion Large tidal volume ventilation can induce acute lung injury. MMP-2 and MMP-9 play an important role in the development of ventilator induced lung injury and the imbalance between MMPs and TIMPs contributes to the mechanism of ventilator-induced lung injury.
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Objective To investigate the effect of acute lung injury (ALI) on ?-defensin-2 (RBD-2) gene expression in rat lung. Methods Sixty SD male rats weighing 250-300g were randomly divided into two groups of 30 animals each: control group and ALI group. Animals were anesthetized with intraperitoneal 5% phenobarbital 120mg?kg-1 . In ALI group acute lung injury was induced with LPS 200 ?g?kg-1 iv. Lungs were harvested before (0h) and 6h, 18h, 1d, 3d and 5d after LPS stimulation. Total RNA was extracted from pulmonary tissue and RBD-2 mRNA was measured by reverse transcription polymerase chain reaction(RT-PCR). GAPDH was used as internal standard. DNA sequencing was used to confirm the specificity of RBD-2 cDNA fragment. Results Acute lung injury induced by intravenous LPS was confirmed by microscopic pathological examination. The level of RBD-2 mRNA in rat lung was 0.77?0.14 in control group. There were no significant changes in pulmonary RBD-2 mRNA expression at different time intervals in control group. In ALI group the RBD-2 mRNA expression at 6h after LPS stimulation was not significantly different from that in control group, whereas a marked increase in pulmonary RBD-2 mRNA was found at 12h and on 1d, 3d and 5d after LPS stimulation as compared with that in control group.Conclusions ?-defensin-2 gene expression shows a constitutive expression pattern. ALI can upregulate the ?-defensin-2 gene expression. The upregulation of ?-defensin-2 gene expression may be involved in the pathogenesis of ALI
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Objective To investigate the effect of partial liquid ventilation(PLV) with perfluorocarbon(PFC) on pulmonary surfactant during beatment of acute lung injury(ALI) induced by oleic acid. MethodsTwenty-four male Japanese white rabbits weighing 2. 1-2.6 kg were randomly divided into three groups(n = 8 ineach group): groupl: normal animal + mechanical ventilation (MV); group 2: ALI + MV; group 3: ALI +PLV.The animals were anesthetized with intraperitoneal ketamine 100 mg/kg, trachectomized and mechanicallyventilated (FiO_2 = 1, RR = 35 bpm, I: E = 1: 2, PEEP = 5 cm H_2O, PaCO_2 was maintained at 35-45 mm Hg byadjustment of tidal volume) .In group 2 and 3 ALI was induced by infusion of oleic acid 150?g/kg via centralvenous catheter over 30 min period. ALI was considered established when PaO_2 /FiO_2 was