對意外或自主拔管患者的研究顯示，接受完全機械通氣患者的23％和開始撤機過程患者的69％并不需要重新插管，這表明機械通氣患者的撤機存在被延遲的傾向，致使患者承受不必要的痛苦，增加了并發癥的發生率和醫療費用。撤機過程所耗費的時間占機械通氣整個時間的40％~50％ 。Esteban等的研究證明：延長通氣時間增加病死率。在美國，機械通氣的費用約2 000美元／d，延長通氣者占總機械通氣患者的6％，但卻消耗ICU資源的37％。我國的撤機現狀與之類似，日益增多的撤機困難患者占用各ICU的有限資源，成為醫療費用和床位周轉的沉重負擔。機械通氣撤離的研究亟待加強。
機械通氣領域目前有幾大爭論, 涉及在機械通氣中基本的也是十分重要的問題, 復習和深入探討這些問題, 對了解機械通氣近年的研究進展, 指導機械通氣的臨床實踐很有意義。
過去10 多年來, 急性呼吸窘迫綜合征( ARDS) 的基礎和臨床研究取得了巨大進展, 也暴露了目前臨床上正在應用的ARDS 診斷標準的重要缺陷。近年來已經有多組學者提出了重新制訂ARDS 診斷標準的建議。為今后更好開展前瞻性多中心隨機對照研究( RCT) , 也迫切需要一個診斷新標準來統一和規范病例的選擇。
Objective To investigate the gene expression of beta-defensin-4 (mBD-4) and mBD-6 in acute lung injury (ALI) mouse.Methods Sixty adult mice were randomly divided into a control group and a ALI group.ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) in the ALI group.The control group was treated with same dose of normal saline.The lung tissues were harvested at different time point after stimulation.The expression of mBD-4 and mBD-6 mRNA was measured by real-time quantitative reverse transcription polymerase chain reaction.DNA sequencing was used to confirm the specificity of mBD-4 and mBD-6 cDNA fragment.Results There were no obvious mBD-4 and mBD-6 mRNA expression in mouse lung in the control group at all time points and ALI 6 h group.In the ALI group a marked increasing expression was found on 12 h，1 d and 3 d after LPS stimulation.The mBD-4 mRNA expression was significant higher in the ALI groups of 1 d and 3 d points than that of ALI 12 h group with no obvious difference between each other.There were no significant differences of mBD-6 mRNA expression between ALI groups of 12 h，1 d and 3 d points Conclusion mBD-4 and mBD-6 mRNA is not constitutive expressed in mouse lung and show a up-regulative expression pattern after ALI.
Objective To investigate the influence of chronic alcohol ingestion on the severity of acute lung injury (ALI) induced by oleic acid and lipopolysaccharide (LPS).Methods Thirty-two SD rats were randomly administrated with alcohol or water for 6 weeks，then instilled with oleic acid and LPS to induce ALI or with normal saline as control.Thus the rats were randomly divided into two injury groups [ethanol group and water group] and two control groups [ethanol group and water group] (n=8 in each group). PaO2,Wet to dry lung weight ratio (W/D)，levels of γ-glutamylcysteinylglycine (GSH) and malonaldehyde (MDA) in the lung tissue were measured.Results Compared to corresponding control groups，the PaO2 and GSH significantly decreased，and the lung W/D and MDA level were significantly increased in the injury groups (all Plt;0.05).In the injury groups，the changes of above parameters were more significant in the alcohol group than thoe in the water group (all Plt;0.05)，except the lung W/D with no significant difference.Conclusion Chronic ethanol ingestion was relevalent to oxidation/ antioxidation imbalance and more severe lung injury in rats with severe septic after trauma,which suggests that chronic alcohol abuse could increase the severity of acute lung injury.
Objective To study the effects of two different tidal volume mechanical ventilation on lipopolysaccharide( LPS) -induced acute lung injury( ALI) , and explore the effects of glutamine on ALI.Methods Thirty male Sprague-Dawley rats were randomly divided into three groups. After anesthesia and tracheotomy were performed, the rats were challenged with intratracheal LPS ( 5mg/kg) and received ventilation for 4 hours with small animal ventilator. Group A received conventional tidal volume, while groupB received large tidal volume. Group C received large tidal volume as well, with glutamine injected intravenously 1 hour before ventilation. Arterial blood gases were measured every one hour. 4 hours later, the rats were killed by carotid artery bleeding. The total lung wetweightwas measured and lung coefficient ( total lung wet weight /body weight ×100) was counted. WBCs and neutrophils in BALF were counted. Protein concentration, TNF-α, IL-6, and cytokine-induced neutrophil chemoattractant-1 ( CINC-1) levels in BALF,myeloperoxidase ( MPO) , and superoxide dismutase ( SOD) levels in the lung were assayed respectively.Results PaO2 and SOD levels decreased more significantly in group B than those of group A. The lung coefficient, WBCs, neutrophils, protein, TNF-α, IL-6, and CINC-1 levels in BALF, MPO levels in lung increased more significantly in group B than those of group A. PaO2 and SOD levels were significantly higher in group C than those of group B. The lung coefficient, WBCs, neutrophils, protein, TNF-α, IL-6, and CINC-1 levels in BALF,MPO levels in lung were significantly lower in group C than those of group B. Conclusion Large tidal volume mechanical ventilation aggravates LPS-induced ALI, and glutamine has obviouslyprotective effects.
Objective To study the effects of hyperoxia on ventilator-induced lung injury（VILI） in rats.Methods 48 healthy male SD rats were randomly divided into four groups：Group A received conventional mechanical ventilation（VT=8 mL/kg） with room air，Group B received the same tidal volume as group A with 100% O2，Group C received large tidal volume（VT=40 mL/kg） with room air，group D received the same tidal volume as group C with 100% O2.Arterial blood gases were measured every one hour and oxygenation index（PaO2/FiO2） was calculated.The changes of lung histopathology were assessed by HE staining and observed under light microscope.Wet-to-dry weight ratio（W/D） of left lung，neutrophils and white blood cell（WBC） counts in BALF were measured.TNF-α，IL-1β，and MIP-2 levels in BALF，malondialdehyde（MDA），myeloperoxidase（MPO），and superoxide dismutase（SOD） levels in the lung were assayed，respectively.Results Compared with the Group C，the Group D demonstrated more infiltrating neutrophils in the lung and more destructive changes in the alveolar wall.Meanwhile，the oxygenation index decreased，the WBC and neutrophils counts in BALF increased，and the W/D of left lung was higher in the Group D with significant differences compared with the Group C.Moreover，the BALF levels of TNF-α，IL-1β and MIP-2，the lung levels of MDA increased，and the lung levels of SOD decreased significantly in the Group D compared with those in the Group C.There were no statistical significant differences between the Group B and Group A in all parameters except that MDA levels increased and SOD levels decreased significantly in the Group B.Conclusion Hyperoxia can increase lung injury induced in large tidal volume ventilation in rats，but has mininmal effects in conventional mechanical ventilation.
Objective To explore the expression and effect of heme oxygenase-1 ( HO-1) in ventilator-induced lung injury. Methods Twenty-four New Zealand rabbits were randomly assigned to three groups, ie. a conventional ventilation + PEEP group( C group) , a ventilator-induced lung injury group( VILI group) , and a VILI + HO-1 inducer hemin group( Hm group) .Western blot and immunohistochemistry assay were used to investigate the expression of HO-1 protein. Blood gas analysis, lung wet /dry ratio, lunghistopathology and lung injury score were used to evaluate lung injury. Results HO-1 protein expression significantly increased in the VILI group compared with the C group. HO-1 was found mainly in alveolar epithelial cells and vascular endothelial cells, as well as in alveolar macrophages and neutrophils. Compared with the VILI group, HO-1 protein and PaO2 /FiO2 increased, while lung wet/dry ratio and lung injury score decreased in the Hmgroup significantly( P lt;0. 05) . Conclusion High HO-1 expression can alleviate lung injury from large tidal volume ventilation, implying its protective role in lung pathogenesis.
Objective To determine the risk factors for acute lung injury（ALI） early after orthotopic liver transplantation.Methods The perioperative clinical data of all 275 patients who had undergone orthotopic liver transplantation were analysed retrospectively.Several statistically significant risk factors were screened out with univarite analysis，then independent risk factors were determined with multivariate stepwise logistic regression analysis.Results Of the all 275 patients，the morbidity of ALI was 9.8% with a mortality of 22.2%.Univariate analysis showed that the occurrence of ALI was associated with preoperative infection，severe hepatitis，renal dysfunction，massive blood transfusion in operation，long non-hepatic period and long cold ischemic time.Multivarite stepwise logistic regression analysis revealed that the independent risk factors for ALI were massive blood transfusion in operation（OR=12.12，95%CI 0.958-25.364），longer non-hepatic period（OR=1.23，95%CI 1.034-1.410） and longer cold ischemic time（OR=22.35，95%CI 1.266-43.421）.Conclusion Massive blood transfusion in operation，long non-hepatic period and long cold ischemic time were independent risk factors for ALI early after orthotopic liver transplantation.
Ojective To establish a rat model of hyperoxia induced acute lung injury. Methods Eighty healthy male SD rats were randomly divided into an air group and a hyperoxia group ( ≥95% O2 ) .Each group was further divided into 12 h, 24 h, 36 h, 48 h, 60 h subgroups. Arterial blood gas was monitored. Lung tissue was sampled for evaluation of lung wet to dry ratio, lung index, and pulmonary permeation index. Bronchoalveolar lavage fluid ( BALF) was collected for measurement of lactatedehydrogenase ( LDH) activity and white blood cell count ( WBC) . Results After hyperoxia exposure for 48 ～60 h, lung pathology showed alveolar structure disruption, lung parenchyma wrath bleeding and edema.Lung wet to dry ratio, lung index, pulmonary permeation index, LDH and WBC in BALF all increased significantly, peaked at 48 h and remained at high level at 60 h while PaO2 dropped progressively.Conclusion Exposure to ≥ 95% O2 for 48 ～60 h can successfully establish the rat model of hyperoxia induced acute lung injury.