Dietary Protein Requirement of Juvenile Dotted Gizzard Shad Konosirus punctatus Based on the Variation of Fish Meal.

An 8-week feeding trial was conducted to investigate the effects of dietary protein levels on growth performance, feed utilization, and energy retention of juvenile dotted gizzard shad Konosirus punctatus based on the variation of fish meal. Fish meal was used as the sole protein source; five semi-purified diets were formulated with varying crude protein (CP) levels of 22.52%, 28.69%, 34.85%, 38.84%, 45.78% (CP1-CP5 diets). A total of 300 uniform juveniles with initial body weight 3.61 ± 0.20 g fish-1 were randomly divided into five groups with three replicates in each group. The results showed that different CP levels did not significantly affect the survival of juvenile K. punctatus (p > 0.05). The values of weight gain (WG) and specific growth ratio (SGR) showed a general enhancing trend and then weakened with increasing dietary CP levels (p > 0.05). Feed utilization also improved with increasing dietary CP levels (p > 0.05), and the optimal feed conversion ratio (FCR) value was found in fish fed the diet with CP3 (p > 0.05). The rise of dietary CP from 22.52% to 45.78% enhanced the daily feed intake (DFI) and protein efficiency ratio (PER) values of K. punctatus (p < 0.05). With the increase of dietary CP levels, daily nitrogen intake (DNI), energy retention (ER), and lipid retention (LR) elevated, while retention (NR), daily energy intake (DEI), and daily lipid intake (DLI) reduced (p < 0.05). No statistical differences in the content of water, crude protein, and crude lipid were observed among different treatments (p > 0.05). The activity of lipase in CP3 and CP4 diets was significantly higher than that of the CP1 diet (p < 0.05). Fish fed CP2 and CP3 diets had significantly higher amylase activity than that of the CP5 diet (p < 0.05). The levels of alanine aminotransferase (GPT) first enhanced and then decreased as dietary CP levels raised. The second-order polynomial regression model analysis of the WG and FCR indicated that the optimal dietary protein level for K. punctatus is about 31.75-33.82% based on the variation of fish meal.

[The role of polymorphonuclear cells in lung ischemia-reperfusion injury in a canine model of pulmonary thromboembolism].

OBJECTIVE: To explore the effects of polymorphonuclear cells (PMN) on lung ischemia-reperfusion (I/R) injury in a canine model of pulmonary thromboembolism. METHODS: Fifteen dogs were divided into three groups: a sham group (n = 5), an ischemia group (n = 5) and a reperfusion group (n = 5). PMN in the whole blood were isolated with density gradient centrifugation. Apoptosis rates of the PMN was measured through flow cytometer after the cells were labeled by Annexin V-FITC before embolectomy and at 2, 4, 6 h after the operation. The myeloperoxidase (MPO) concentrations in lung homogenates were measured by ELISA. Alveolar PMN in the reperfusion lobar were observed by optical microscopy. The lung ultrastructure was studied by transmission electron microscopy. RESULTS: Alveolar PMN infiltration and the concentrations of MPO in the reperfusion group were significantly higher than those in the ischemia group (PMN (31 +/- 11) vs (8 +/- 4)/ten high power fields, MPO (11.7 +/- 1.6) vs (9.1 +/- 0.5) microg/L, P < 0.05). In the reperfusion group, abundant inflammatory cell infiltration was observed, predominantly with PMN in the alveoli. Apoptosis rates of the blood PMN at 6 h after reperfusion were much lower than before reperfusion (3.0 +/- 2.5)% vs (7.4 +/- 4.5)%, P < 0.05). At 4 and 6 h after operation, the PMN apoptosis rates in the reperfusion group were significantly lower than the ischemia group (4 h: (4.8 +/- 2.6)% vs (9.3 +/- 2.0)%, 6 h: (3.0 +/- 2.5)% vs (8.0 +/- 1.6)%, P < 0.05). PMN attaching firmly to the alveolar septum were observed by electron microscope. CONCLUSION: PMN with enhanced activities and decreased apoptosis rate, are involved in the cellular mechanisms of the lung I/R injury in this model of pulmonary thromboembolism.

[Relationship between polymorphisms of plasminogen activator inhibitor-1 promoter gene and pulmonary thromboembolism in Chinese Han population].

OBJECTIVE: To determine the prevalence of polymorphisms in the plasminogen activator inhibitor-1 (PAI-1) promoter 4G/5G polymorphisms in Chinese Han population and to investigate whether they are associated with pulmonary thromboembolism (PTE). METHODS: Samples of peripheral venous blood were collected from 101 patients with PTE diagnosed by high probability of lung ventilation/perfusion scan and/or multi-slice CT pulmonary angiography (CTPA) as well as medical history and clinical manifestations, 67 males and 34 females, aged 48 +/- 15, and 101 age and sex-matched healthy controls from the same geographic area as controls. The genome DNA was extracted from the whole blood using potassium iodide-phenol-chloroform method. Polymerase chain reaction (PCR), denaturing high performance liquid chromatography (DHPLC), and sequence analysis were used to screen the single nucleotide polymorphisms and the genotype distribution of -675 4G/5G located in the promoter region of the PAI-1 gene. RESULTS: The frequencies of the allele 4G of PAI-1 gene in the controls were 0.495, significantly lower than in the PTE patients (0.733, chi(2) = 24.060, P < 0.01). The frequencies of the allele 5G of PAI-1 gene in the controls were 0.505, significantly higher than that in the PET patients. The genotype frequency of 4G4G of the PET patients was 57.4%, significantly higher than that of the controls (30.7%, P = 0.000). The genotype frequencies of 4G5G and 5G5G of the PET patients were 31.7% and 10.9% respectively, not significantly different from those of the controls (37.6 and 31.7% respectively). The presence of 4G allele of PAI-1 gene was found to be a greater risk factor for PTE. In comparison with the controls, the OR of 4G4G + 4G5G, 4G4G, and 4G5G in the PET patients were 3.794 (1.786 - 8.060), 5.443 (2.416 - 12.260), and 2.450 (1.067 - 5.623) respectively with the P values of 0.001, 0.000, and 0.035 respectively. CONCLUSION: The 4G/5G and 4G/4G genotypes are associated with the pathogenesis of PET.T.

[Effects of different durations of thromboembolism on blood gases, hemodynamics, pulmonary arteriography and thrombo-pathology in a canine model with selective embolization of pulmonary lobar arteries].

OBJECTIVE: To investigate the effects of different durations of thromboembolism on blood gases, hemodynamic parameters, pulmonary arteriography and thrombo-pathology in an animal model mimicking chronic pulmonary thromboembolism (PTE). METHODS: Sixteen dogs were embolized with five thrombi developed by autologous blood into the left lower pulmonary artery (n = 15) and the right lower pulmonary artery (n = 1, used to confirm the available method of selective embolization). The 15 dogs were divided into three groups: sham group (n = 5), one-week group (n = 5) and two-week group (n = 5) according to the different durations of embolization. Swan-Ganz catheter was used to guide a plastic duct, through which the thrombi were injected selectively into the left or right lower pulmonary artery by X-ray fluoroscopy. Local pulmonary arteriography of lower pulmonary arteries was taken. Blood pressure (BP), and blood gases were measured. Central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), pulmonary arteriole wedge pressure (PAWP), and cardiac output (CO) were recorded, and pulmonary vascular resistance (PVR) was calculated. Each dog underwent muscular injection with tranexamic acid for one or two weeks to prevent thrombolysis. The lower lung lobe was dissected to confirm the thromboembolism after one or two weeks. The lung sections were stained with phosphotungstic acid hematoxylin (PTAH) to observe thromboemboli with optical microscopy. RESULTS: In the PTE group, PaO(2)/FiO(2), MPAP and PVR changed significantly as compared to baseline values (P < 0.05) after one hour of embolization, with MPAP increasing from (15 +/- 3) mm Hg to (21 +/- 4) mm Hg, PVR increasing from (178 +/- 114) mm Hg.s/L to (404 +/- 260) mm Hg.s/L, and PaO(2)/FiO(2) decreasing from (508 +/- 58) mm Hg to (395 +/- 100) mm Hg; these parameters returned to the baseline values one or two weeks later. After embolization, pulmonary arteriography demonstrated lower lobar artery cut-off perfusion defects. One week later, pulmonary arteriography demonstrated irregularities and stiffness of the arterial wall, enlarged proximal part of lower pulmonary artery and cut-off perfusion defects. Poor filling at embolus site was evident after embolization for two weeks. In the 1-week PTE group, organized tissue covered with the blue-purple fibrin nest was observed in the thrombus with PTAH stain. In the two-week group, the well organized thrombi were partially recanalized and surrounded and invaded by hyperplastic tissues from pulmonary artery wall. CONCLUSIONS: A canine model mimicking chronic PTE can be established by the use of fibrinolytic inhibitor tranexamic acid. Different manifestations on pulmonary arteriography and varied degree of organization of thrombi are evident at different times after embolization.

[The effect of VEGF antisense oligonucleotides combined with low molecular weight heparin on the growth and metastasis of mice Lewis lung cancer].

OBJECTIVE: To investigate the inhibitory effect of vascular endothelial growth factor (VEGF) antisense oligonucleotides or/and dalteparin sodium (fragmin) on tumor growth and metastasis of mice Lewis lung cancer. METHODS: 40 mice with Lewis lung cancer were randomizedly divided into five groups: control group, VEGF antisense oligonucleotides (ASODN) group, VEGF mismatch sense oligonucleotides (MSODN) group, low molecular weight heparin (LMWH) group, and combined group. Sodium chloride, VEGF-ASODN, VEGF -MSODN, fragmin, and VEGF-ASODN plus fragmin were given respectively (once every two days, 15 times altogether). The volume and weight of subcutaneous tumors were measured, and the rates of lung metastasis were detected by HE staining. The microvessel density (MVD) in tumor mass were measured by immunohistochemistry staining. VEGF protein level in tumor tissue were detected by Western blot assay. RESULTS: After treatment, the tumor growth inhibitory rates were 47.34%, 27.31% and 59.03%, and the rates of lung metastasis were 37.5%, 37.5% and 25% in ASODN, LMWH, and the combined group, respectively. Tumor MVD and VEGF protein expression of the above three groups were lower than those of the control group. There was a significant difference in regard to the tumor growth inhibitory rates and MVD between the above three treated groups and the control group as well as the MSODN group (P < 0.05). CONCLUSIONS: VEGF-ASODN and fragmin may down-regulate VEGF gene expression and inhibit angiogenesis, Combined use of fragmin can enhance anti- tumor effect of VEGF-ASODN.

Relationship between polymorphisms of genes encoding microsomal epoxide hydrolase and glutathione S-transferase P1 and chronic obstructive pulmonary disease.

BACKGROUND: Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). However, only 10% - 20% of chronic heavy cigarette smokers develop symptomatic disease. COPD is most likely the result of complex interactions between environmental and genetic factors. Genetic susceptibility to COPD might depend on the variations in enzyme activities that detoxify cigarette smoke products, such as microsomal epoxide hydrolase (mEH) and glutathione S-transferase (GST). In this study, we investigated the relationship between polymorphisms in the genes encoding mEH and glutathione S-transferase P1 (GSTP1) and COPD in a Chinese population. METHODS: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to find mEH polymorphism in exon 3 (Tyr113-->His), exon 4 (His139-->Arg) and GSTP1 polymorphism in exon 5 (Ile105-->Val) in 100 COPD patients and 100 age- and sex-matched healthy controls. RESULTS: The proportion of mEH exon 3 heterozygotes was significantly higher in patients with COPD than that in the control subjects (42% vs 32%). The odds ratio (OR) adjusted by age, sex, body mass index (BMI) and cigarette years was 2.96 (95% CI 1.24 - 7.09). There was no marked difference in very slow activity genotype versus other genotypes between COPD patients and the controls. When COPD patients were non-smokers, the OR of very slow activity genotype versus other genotypes was more than 1.00; and when COPD patients were smokers (current smokers and ex-smokers), the OR was less than 1.00. There was no significant difference in GSTP1 polymorphism adjusted by age, sex, BMI and smoking between COPD patients and the controls. CONCLUSIONS: mEH exon 3 heterozygotes might be associated with susceptibility to COPD in China. The interaction might exist between mEH genotype and smoke. The gene polymorphism for GSTP1 might not be associated with susceptibility to COPD in the Chinese population.

[Experimental study of the thrombolytic effects in a canine model of pulmonary thromboembolism induced by autologous radioactive blood clots].

OBJECTIVE: To compare the thrombolytic effects of the two dosing regimes with urokinase (UK) in a canine model of pulmonary thromboembolism induced by radioactive blood clots. METHODS: Seventeen dogs were randomly assigned into three groups: the control group, the UK(2h) group (UK infused over 2 hours) and the UK(12h) group (UK given over 12 hours). The thrombolytic differences was investigated among the three groups. Thrombolysis was assessed by continuously counting over both lung fields with single photon emission computed tomography (SPECT) and calculated by regions of interest (ROI) technology and by counting radioactivity in the lung in vitro. The extent of thrombolysis was calculated as the difference between the radioactivity originally incorporated in the clot (decay-corrected) and the radioactivity in the lung in vitro. RESULTS: In three groups, the lysis rates measured by ROI technology were (6.2 +/- 4.0)%, (39.5 +/- 13.9)%, and (16.9 +/- 8.9)% respectively, and (6.0 +/- 2.7)%, (42.8 +/- 12.4)%, and (17.7 +/- 9.3)% by the method in vivo. The thrombolytic ratio of the UK(2h) group was significantly higher than that of the other two groups (P < 0.01), and there was no marked difference between the control group and the UK(12h) group. There was a thrombolytic peak in the UK(2h) group at the first four hours after infusion of agent. CONCLUSIONS: For the fresh thrombi, the UK(2h) regime is superior to the UK(12h) due to its higher thrombolytic ratio and prompt thrombolytic property. The model and methods are highly reliable.

[Association between polymorphisms in the microsomal epoxide hydrolase (mEH) gene and chronic obstructive pulmonary disease].

OBJECTIVE: To investigate the association between polymorphisms in the microsomal epoxide hydrolase (mEH) gene and susceptibility to chronic obstructive pulmonary disease (COPD) in a Chinese population. METHODS: Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to genotype mEH polymorphisms in exon3 (Tyr113-->His) and exon4 (His139-->Arg) in 100 COPD patients and 100 age and sex matched healthy controls. RESULTS: (1) The proportion of mEH heterozygotes in exon3 was significantly higher in the patients with COPD than that in the control subjects (42% vs 32%). The odds ratio (OR) adjusted by age, sex, body mass index (BMI) and cigarettes years was 2.96 (95% CI 1.24 - 7.09). (2) There was no marked difference in very slow activity genotype versus other genotypes between COPD patients and controls. (3) When COPD patients were nonsmokers, the OR of very slow activity genotype versus other genotypes was more than 1.00, and when COPD patients were smokers (Current smokers and ex-smokers), the OR was less than 1.00. CONCLUSIONS: (1) mEH heterozygotes in exon3 might be associated with the susceptibility to COPD in China. (2) The interaction might be existed between mEH genotype and smoke.

[Association between polymorphisms in the gene coding for glutathione S-transferase P1 and chronic obstructive pulmonary disease].

OBJECTIVE: To investigate the association between polymorphisms in the gene coding for glutathione S-transferase P1 (GSTP1) and susceptibility to chronic obstructive pulmonary disease (COPD) in a Chinese population. METHODS: This was a pilot study of the molecular epidemiology in patients with COPD. The research design was a case-control study. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to genotype GSTP1 polymorphisms in exon 5 in 100 COPD patients and 100 age and sex matched healthy controls. Logistic regression analysis method was used to calculate the odds ratio (OR) and the 95% confidence interval (CI). RESULT: There was no significant difference in GSTP1 polymorphisms adjusted by age, sex, body mass index and smoking between COPD patients and controls. CONCLUSION: The gene polymorphism for GSTP1 was not associated with susceptibility to COPD in the Chinese population.

[A canine model of acute pulmonary thromboembolism induced by autologous radioactive blood clots].

OBJECTIVE: To establish a canine model of pulmonary thromboembolism (PTE) for evaluating the effects of thrombolytic therapy. METHODS: The preparations of radioactive blood clots in vitro were made from fresh whole blood (from 6 donors) mixed with (99m)Tc-SC. After eluting the clots with saline solution, the stability and evenness of (99m)Tc-SC in the clots were determined. Then a canine model of PTE induced by these clots was established and the rates of spontaneous lysis were measured by the regions of interest (ROI) technique and the in vitro method. RESULTS: (99m)Tc-SC was stable in the radioactive blood clots after elution, and the radioactivities in the thrombi were well-distributed. The rates of thrombolysis were (6.2 +/- 4.0)% as measured by ROI and (6.0 +/- 2.7)% by the in vitro method. CONCLUSIONS: (99m)Tc-SC is stable and well-distributed in blood clots. A canine model of PTE can be induced by autologous radioactive blood clots.

Beta-carotene protects rats against bronchitis induced by cigarette smoking.

OBJECTIVE: To investigate the protective effects of beta-carotene in rats against the development of chronic bronchitis induced by cigarette smoking. METHODS: Forty-two Male Wistar rats were randomly divided into three study groups: (1) control (n = 15), animals underwent no treatment; (2) cigarette smoking (n = 15), animals developed chronic bronchitis through long-term cigarette smoking twice a day for 75 d; (3) beta-carotene plus cigarette smoking animals (n = 12) were given 1 ml or 15 mg/kg beta-carotene orally every day just before cigarette smoking. The levels of IL-6, IL-8, NO, superoxide dismutase (SOD) and lipoperoxide (LPO) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were measured and the pathological changes to lung tissue were analyzed using light microscopy. RESULTS: Long-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. beta-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis. CONCLUSIONS: Quantitative oral intake of beta-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

[Expression of matrix metalloproteinases in lung tissue and levels of some cytokines in bronchoalveolar lavage fluid in the obstructive emphysema rat models].

OBJECTIVE: To observe the changes of matrix metalloproteinase-2 (MMP-2), MMP-9 and interleukin-10 (IL-10), tumor necrosis factor-alpha (TNFalpha) in lung tissue of the obstructive emphysema rat models and to evaluate the relationship between these changes and emphysema formation. METHODS: The rat emphysema models were established by exposure to cigarette smoking. Pulmonary function tests were performed to evaluate the forced expiratory volume in 0.3 second (FEV(0.3)), FEV(0.3)/forced vital capacity (FVC) and functional residual capacity (FRC). The morphological indices of emphysema were measured by computer image analyzer. The protein expression and enzymatic activity of MMPs in lung tissue were observed. The contents of IL-10 and TNFalpha in bronchoalveolar lavage fluid (BALF) were measured. RESULTS: Pulmonary function test showed that in model group the FEV(0.3)/FVC was decreased, whereas the FRC was increased significantly than those in control group (P < 0.01, respectively). There was a significant decrease in the relative content of elastin in lung tissue in model group than that in control group. The expression and enzymatic activity of MMP-2 and MMP-9 in lung tissue, the counts of total leukocytes and neutrophils and the level of TNFalpha in BALF were significantly elevated, but the level of IL-10 in BALF was significantly reduced in model group compared with those in control group (P < 0.01, respectively). There were statistically significant positive correlations between the enzymatic activity of MMP-2, MMP-9 and the total leukocyte counts (P < 0.01, respectively), and significant negative correlations between the enzymatic activity of MMP-2, MMP-9 and the content of elastin (P < 0.05, respectively). CONCLUSIONS: MMP-2, MMP-9, IL-10 and TNFalpha may play an important role in the formation of obstructive emphysema in rat models caused by passive smoking.

Sequential non-invasive mechanical ventilation following short-term invasive mechanical ventilation in COPD induced hypercapnic respiratory failure.

OBJECTIVE: To estimate the feasibility and the efficacy of early extubation and sequential non-invasive mechanical ventilation (MV) in chronic obstructive pulmonary disease (COPD) with exacerbated hypercapnic respiratory failure. METHODS: Twenty-two intubated COPD patients with severe hypercapnic respiratory failure due to pulmonary infection (pneumonia or purulent bronchitis) were involved in the study. At the time of pulmonary infection control window (PIC window) appeared, when pulmonary infection had been significantly controlled (resolution of fever and decrease in purulent sputum, radiographic infiltrations, and leukocytosis) after the antibiotic and the comprehensive therapy, the early extubation was conducted and followed by non-invasive MV via facial mask immediately in 11 cases (study group). Other 11 COPD cases with similar clinical characteristics who continuously received invasive MV after PIC window were recruited as control group. RESULTS: All patients had similar clinical characteristics and gas exchange before treatment, as well as the initiating time and all indices at the time of the PIC window. For study group and control group, the duration of invasive MV was (7.1 +/- 2.9) vs (23.0 +/- 14.0) days, respectively, P < 0.01. The total duration of ventilatory support was (13 +/- 7) vs (23 +/- 14) days, respectively, P < 0.05. The incidence of ventilator associated pneumonia (VAP) were 0/11 vs 6/11, respectively, P < 0.01. The duration of intensive care unit (ICU) stay was (13 +/- 7) vs (26 +/- 14) days, respectively, P < 0.05. CONCLUSIONS: In COPD patients requiring intubation and MV for pulmonary infection and hypercapnic respiratory failure, early extubation followed by non-invasive MV initiated at the point of PIC window significantly decreases the invasive and total durations of ventilatory support, the risk of VAP, and the duration of ICU stay.

[The pathology of and the cardio-pulmonary functional changes in acute multiple pulmonary microthromboembolism in a canine model].

OBJECTIVE: To evaluate the effect of acute multiple pulmonary microthromboembolism on circulation, ventilation, lung histology, and the coagulatory and fibrinolytic functions. METHODS: Thirteen dogs were studied, 7 in the embolism group and 6 in the control group. 10 ml of blood was withdrawn from each animal. Thrombi were formed and cut into pieces of 1 mm to 2 mm in size. The thrombi were counted, and 300 thrombi were infused at one time back to the same animal. PAP, PAWP, VO(2), DO(2), D-dimer, protein C, protein S were measured before and immediately, 30 min, 1 hour, 2 hour after embolism. RESULTS: PAP was increased immediately after embolisation, and then decreased at 1 hour. The level of D-dimer was elevated at an early stage. Pulmonary hemorrhage, consolidation and microembolism were observed. CONCLUSIONS: Multiple microthromboembolism caused lung injury and thrombosis. PAP was increased at the early stage, but ventilation was not affected. The level of D-dimer changed at the early stage of thromboembolism.

Proportional assist ventilation: methodology and therapeutics on COPD patients compared with pressure support ventilation.

OBJECTIVE: To investigate the impact of proportional assist ventilation (PAV) on tolerance and breathlessness in ventilated chronic obstructive pulmonary disease (COPD), and to describe the patient-ventilator interaction, hemodynamic state, breathing pattern and work of breath during PAV and pressure support ventilation (PSV). METHODS: Ten intubated COPD patients on weaning from mechanical ventilation were studied. Elastance and resistance were measured by both the inspiratory-hold technique during a brief period of volume control ventilation and runaway technique during PAV. Each assistance level of PAV (80%, 60% and 40%) and PSV was selected randomly. Patients' response, hemodynamics, blood gas and lung mechanics were monitored. RESULTS: Tidal volume and respiratory rate didn't change in a consistent manner as the level of assist was decreased (P > 0.05). With the level of assist increasing, peak inspiratory pressure was increasing significantly (P < 0.05), while patients' work of breath had the tendency to decrease (P < 0.05). A significant difference in the Borg Category Scale was observed between PAV and PSV (0.50 [1.50] vs. 0.75 [2.00], P < 0.05) at the same degree of respiratory muscle unloading. PaCO(2) was significantly higher on PAV (54 [23] mm Hg) than on PSV (48 [23] mm Hg) (P < 0.05). Peak inspiratory pressure on PAV was significantly lower than on PSV (16 +/- 4 cm H(2)O vs. 21 +/- 3 cm H(2)O, respectively, P < 0.05). Hemodynamics and oxygenation remained unchanged. CONCLUSIONS: PAV is a feasible method for supporting ventilator-dependent patients and was well tolerated. It can improve the breathing pattern and reduce inspiratory effort. At the same degree of respiratory muscle unloading, PAV can be implemented at much lower peak inspiratory pressure than PSV. It can also apply proportional pressure support according to the patients' ventilatory demand.