Objective To investigate the effects of different levels of intra-abdominal pressure ( IAP) on respiration and hemodynamics in a porcine model of acute lung injury( ALI) .Methods A total of 8 domestic swine received mechanical ventilation. Following baseline observations, oleic acid 0. 1mL/kg in 20mL of normal saline was infused via internal jugular vein. Using a nitrogen gas pneumoperitongum, the IAP increased from0 to 15 and 25mmHg, and the groups were named IAP0 , IAP15 and IAP25 , respectively. During the experimental period, hemodynamic parameters including heart rate ( HR) , cardiac output ( CO) , mean arterial pressure( MAP) , central venous pressure( CVP) , intrathoracic blood volume index( ITBVI) and so on were obtained by using thermodilution technique of pulse induced continuous cardiac output( PiCCO) . The esophageal pressure( Pes) was dynamicly monitored by the esophageal catheter. Results Pes and peak airway pressure( Ppeak) increased and static lung compliance( Cstat) decreased significantly in IAP15 and IAP25 groups compared with IAP0 group( all P lt;0. 01) . Transpulmonary pressure( Ptp) showed a downward trend( P gt;0. 05) . PO2 and oxygenation index showed a downward trend while PCO2 showed a upward trend ( P gt;0. 05) . HR and CVP increased significantly, cardiac index( CI) and ITBV index decreased significantly ( all P lt;0. 05) ,MAP didn′t change significantly( P gt;0. 05) . The changes in Pes were negatively correlated with the changes in CI( r = - 0. 648, P = 0. 01) . Conclusion In the porcine model of ALI, Pes increases because of a rise in IAP which decreased pulmonary compliance and CI.
Objective To observe whether additional penehycl idine hydrochloride (PHC) in mechanical ventilation produces therapeutic effect on oleic acid (OA) induced acute lung injury (ALI) in canine. Methods Seventeen male canines (weighing 12-17 kg) were divided into control group (n=5), OA group (n=6) and PHC group (n=6). ALI model was developed by central venous injection of OA in canines of OA and PHC groups. ALI model was kept steady in air, all groups received mechanical ventilation 90 minutes later. Three groups received normal sal ine 0.25 mg/kg without injection of OA(control group), normal sal ine 0.25 mg/kg after injection of OA (OA group) and PHC 0.25 mg/kg after injection of OA (PHCgroup) respectively at 0 h (90 minutes after onset time of ALI/ARDS). The heart rate (HR), mean arteial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), artery blood gas analysis, cardiac output (CO), extravascular lung water index (EVLWI), FiO2 and VT were observed respectively at basel ine, onset time of ALI/ARDS and 0 h, then again at 1 hour intervals for 6 hours. Besides the above, airway peak pressure (Ppeak), airway plat pressure (Pplat), mean airway pressure (Pmean) and positve end-expriatory pressure (Peep) were also observed each hour during 1-6 hours. Oxygenation index (OI), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), alveolar-arterial differences for O2 (AaDO2) and dynamic lung compl iance (DLC) were calculated and pulmonary tissue was collected for histopathologic investigation and dry wet weight ratio (WDR) test. Results The functional parameters of PHC group were improved when compared those of OA group, but there was no siginficant difference; WDR of independent region of three groups were 80.42% ± 3.48%, 82.67% ± 4.01% and 82.26% ± 1.43% respectively; WDR of dependent region of three groups were 80.51% ± 3.60%, 83.71% ± 1.98% and 82.57% ± 1.08% respectively. WDR of PHC group were obviously improved when compared with those of OA group, but there was no significant difference. Independent and dependent regions of PHC group were significantly improved when compared those of OA group in histopathologic scores, alveolar edema, inflammatory infiltration and over-distension (P lt; 0.01). Conclusion Additional PHC in mechanical ventilation produces obvious therapeutic effect on OA induced acute lung injury in canine.
ObjectiveTo explore the clinical value of three early predictive scale of lung injury (ALI) in patients with high risk of acute lung injury (ALI) after lung cancer surgery.MethodsA convenient sampling method was used in this study. A retrospective analysis was performed on patients with lung cancer underwent lung surgery. The patients were divided into an ALI group and a non-ALI group according to ALI diagnostic criteria. Three kinds of lung injury predictive scoring methods were used, including lung injury prediction score (LIPS), surgical lung injury prediction (SLIP) and SLIP-2. The differences in the scores of the two groups were compared. The correlation between the three scoring methods was also analyzed. The diagnostic value was analyzed by drawing receiver operating characteristic (ROC) curves.ResultsA total of 400 patients underwent lung cancer surgery, and 38 patients (9.5%) developed ALI after operation. Among them, 2 cases progressed to acute respiratory distress syndrome and were treated in intensive care unit. There were no deaths. The predictive scores of the patients in the ALI group were higher than those in the non-ALI group, and the difference was statistically significant (all P<0.001). There was a good correlation between the three scoring methods (allP<0.001). The three scoring methods had better diagnostic value for early prediction of high risk ALI patients after lung cancer surgery and their area under ROC curve (AUC) were larger than 0.8. LIPS score performed better than others, with an AUC of 0.833, 95%CI (0.79, 0.87).ConclusionThree predictive scoring methods may be applied to early prediction of high risk ALI patients after lung cancer surgery, in which LIPS performs better than others.
ObjectiveTo evaluate systematically the relationship between obesity and clinical prognosis in acute respiratory distress syndrome (ARDS) patients.MethodsA systematic search was performed in Pubmed, EMBASE, Cochrane databases, Wiley, Ovid, Medline, CNKI, VIP and Wanfang. All studies that reported obesity in the clinical prognosis of ARDS and acute lung injury were included. A meta-analysis was performed using RevMan 5.0 and Stata 10.0.ResultsA total of 28 368 patients from 9 studies were included in this meta-analysis. The combined results showed that obesity was associated with the decreased mortality of ARDS [odds ratio(OR)=0.63, 95% confidence intervals (95%CI) 0.41 to 0.98, P=0.04]. In subgroup analysis, the result showed no obvious relationship between obesity and 28-day mortality in ARDS/ALI (OR=0.92, 95%CI 0.55 to 1.54, P=0.76). However, obesity was associated with lower risk of 60days and 90-day mortality in ARDS/ALI (60-day: OR=0.84, 95%CI 0.75 to 0.94, P=0.002; 90-day: OR=0.38, 95%CI 0.22 to 0.66, P=0.000 5). Compared with normal weight patients with ARDS, hospital length of stay, ICU length of stay, and duration of mechanical ventilation did not differ significantly [hospital length of stay: weighted mean difference (WMD)=3.61, 95%CI –0.36 to 7.57, P=0.07; intensive care unit (ICU) length of stay: WMD=1.52, 95%CI –0.22 to 3.26, P=0.09; duration of mechanical ventilation: WMD=–0.50, 95%CI –2.18 to 1.19, P=0.56], but ventilator-free days was significantly longer in obese patients (WMD=2.68, 95%CI 0.86 to 4.51, P=0.004).ConclusionsObesity is not associated with hospital length of stay, ICU length of stay, and duration of mechanical ventilation in patients with ARDS. However, obesity is associated with a reduction of long-term mortality and increased ventilator-free days in the patients with ARDS. Additional larger randomized controlled studies are needed to confirm the possible role of obesity in the clinical prognosis of ARDS.
Objective To investigate whether p38 mitogen activated protein kinase (p38MAPK) inhibitor can reduce acute lung injury (ALI) caused by lipopolysaccharide (LPS) by regulating Th17/Treg balance. Methods Balb/c mice were randomly divided into a control group, an ALI group and an intervention group. The mice in the control group were injected with phosphate-buffered saline, the mice in the ALI group were intraperitoneally injected with 40 mg/kg LPS, and the mice in the intervention group were injected with SB203580 (0.5 mg/kg, 1 mg/kg, 2 mg/kg, 5 mg/kg) intraperitoneally 1 h prior to the intraperitoneal injection of LPS. All mice were killed on 12 h later respectively. Hematoxylin-eosinstin staining was used to observe the pathological changes of lung tissue, and cell classification, counting, and total protein levels in bronchoalveolar lavage fluid (BALF) were detected. Transcript expression of forkhead box p3 (Foxp3) and retinoic acid receptor-related orphan receptor-γt (RORγt) was detected by real-time polymerase chain reaction. Interleukin (IL)-6, IL-10, IL-17, IL-23 and transforming growth factor-β (TGF-β) in lung tissue and IL-6, tumor necrosis factor-α (TNF-α) in serum were measured by enzyme-linked immunosorbent assay. The Th17 and Treg subset distribution in spleen was determined by flow cytometry. Results Histopathological examination showed that LPS induced inflammatory cell infiltration in lung tissue, increased cell count and protein levels in BALF (P<0.05), and increased proportion of neutrophils and monocytes in the ALI mice. SB203580 significantly attenuated tissue injury of the lungs in LPS-induced ALI mice. Serum levels of IL-6 and TNF-α in the ALI group were significantly higher than those in the control group, and inflammatory cytokines were decreased after SB203580 intervention. Compared with the ALI group, the production of inflammatory cytokines associate with Th17, including IL-17, IL-23, RORγt was inhibited, and the production of cytokines associate with Treg, such as IL-10 and Foxp3 in lung tissue was increased in the intervention group in a concentration-dependent manner with SB203580. After SB203580 intervention, Th17/Treg ratio was significantly decreased compared with the LPS group (P<0.05). Conclusion p38MAPK inhibitor can reduce LPS-induced ALI by regulating the imbalance of Treg cells and Th17 cells.
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.
Acute lung injury is one of the common and serious complications of acute aortic dissection, and it greatly affects the recovery of patients. Old age, overweight, hypoxemia, smoking history, hypotension, extensive involvement of dissection and pleural effusion are possible risk factors for the acute lung injury before operation. In addition, deep hypothermia circulatory arrest and blood product infusion can further aggravate the acute lung injury during operation. In this paper, researches on risk factors, prediction model, prevention and treatment of acute aortic dissection with acute lung injury were reviewed, in order to provide assistance for clinical diagnosis and treatment.
Objective To observe the effects of exogenous pulmonary surfactant (PS) on ventilation-induced lung injury (VILI) in rats, and to investigate its possible mechanisms. Methods A total of 40 Wistar rats were divided into 4 groups with randomized blocks method: control group, high tidal volume (HV) group, VILI group, and PS group, with 10 rats in each group. The control group was subjected to identical surgical procedure but was never ventilated. After 30 min of mechanical ventilation (MV) with Vt 45 ml/kg, the rats in HV group were killed immediately; rats in the VILI group were continually ventilated for up to 150 min with Vt 16 ml/kg; in the PS group, 100 mg/kg of PS administered intratracheally and with the same settings as VILI group. Mean artery pressure (MAP), blood gas analysis, lung wet to dry weight ratios (W/D), thorax-lung compliance, and cell counts in bronchoalveolar lavage fluid (BALF) were determined. Nuclear factor-κB(NF-κB) activity in lungs was measured by enzyme-linked immunosorbent assay (ELISA), interleukin-8(IL-8) in serum and BALF was determined by radioimmunoassay (RIA). Pathological examination of the lung was performed. Results Injurious ventilation significantly decreased MAP and PaO2/FiO2, but increased NF-κB activity and W/D. MAP and PaO2/FiO2 improved, but NF-κB activity, IL-8 in serum and BALF, and cell counts in BALF reduced significantly in PS group compared with those in VILI group. Histological studies showed reduced pulmonary edema and atelectasis in the PS group. Conclusion PS administered intratracheally can suppress the increased activity of NF-κB induced by VILI, exogenous PS can be used to treat VILI.
Objective To investigate the effect of bilevel ventilation mode on blood gas and hemodynamics of patients with acute lung injury (ALI) by pulse indicator continuous cardiac output(PiCCO), and the clinical effect of this new ventilation mode on patients with ALI as well as its influence degree of circulatory system so that the cure rate of ALI can be improved. Methods There were 42 patients with ALI, 27 male and 15 female aged 15-75 years. According to the order of hospitalization, 40 patients (2 patients did not complete the study) were divided into two groups with 20 patients in each group. Bilevel ventilation group included the first 20 admitted patients. They were given bilevel ventilation support, using Support/Time(S/T) mode. The initial set of end inspiratory pressure (IPAP) was 8-10 cm H2O gradually increased to 14-20 cm H2O, which should be comfortable and appropriate for patients. The initial set of end expiratory pressure (EPAP) was 3-5 cm H2O gradually increased to 8-12 cm H2O. Fraction of inspired oxygen(FiO2) unchanged. Control group included the rest 20 admitted patients. They were given respiratory support, using Auxiliary/Control(A/C) mode followed by an increased positive endexpiratory pressure (PEEP) of 5 cm H2O,10 cm H2O,15 cm H2O,20 cm H2O. Each pressure kept 30 min. FiO2 unchanged. Indexes such as cardiac output (CO), systemic vascular resistance (SVR) etc were observed in both groups. Results There were 13 deaths in two groups, including 5 in bilevel ventilation group and 8 in control group. Seven cases died of multiple organ failure, 3 died of septic shock and 3 died of circulatory failure. Endotracheal intubation time (2.9±0.8 d vs. 4.2±0.9 d, t=7.737, P=0.006) and hospital stay (17.2±4.5 d vs. 18.5±3.6 d, t=2.558, P=0.039) in bilevel ventilation group were significantly shorter than those in control group. In control group, when PEEP ranged from 5 cm H2O to 15 cm H2O, arterial partial pressure of oxygen (PaO2) and oxygenation index (PaO2/FiO2) gradually increased as PEEP increased (Plt;0.05); when PEEP increased to 20 cm H2O, CO decreased, SVR, pulmonary vascular resistance (PVR) and airway peak pressure (PIP) increased than those in range of 515 cm H2O (Plt;0.05). In bilevel ventilation group, PaO2 and PaO2/FiO2 gradually increased as EPAP increased. When EPAP increased to 10 cm H2O, PaO2 and PaO2/FiO2 increased to the maximum (Plt;0.05); PIP was significantly lower than that in control group (t=7.831, .P.=.0.000). Conclusion Giving bilevel ventilation treatment to patients with ALI/acute respiratory distress syndrome(ARDS) can reduce the effects on respiratory and hemodynamic. PIP and the time of endotracheal intubation and hospital stay can be reduced without affecting hemodynamics.
Objective To investigate the effects of noninvasive ventilation for the treatment of acute respiratory failure secondary to severe acute respiratory syndrome ( SARS) . Methods 127 patients with complete information were collected from the database of SARS in Guangdong province, who were all consistent with the ALI/ARDS diagnostic criteria. The patients were divided into three groups depending on ventilation status, ie. a no-ventilation group, a noninvasive ventilation group, and a mechanical ventilation group. The outcome of ventilation treatmentwas followed up.Multi-factor regression analysis was conducted to analyze the relations of ventilation treatment with ARDS and mortality, and factors associated with success of noninvasive ventilation. Results As soon as the patients met the diagnostic criteria of ALI/ARDS, the patients in the noninvasive ventilation group were in more serious condition and had a higher proportion of ARDS compared with the no-ventilation group ( P lt;0. 01) . The patients in the mechanical ventilation group had a higher mortality rate ( P lt;0.01) . 6 and 7 patients in the no-ventilation group had noninvasive ventilation and invasive ventilation thereafter, respectively. 15 patients in the noninvasive group switched to invasive ventilation. Compared with the patients without ventilation ( n =45) , the patients receiving noninvasive ventilation ( n = 61) were in more serious condition and at higher risk of developing ARDS ( P lt;0. 01) , but the mortality was not different between them ( P gt; 0. 05) . The patients who continued to receive noninvasive ventilation ( n = 40) were in more serious condition, and at higher risk of developing ARDS compared with the patients without ventilation ( n = 45) ( P lt; 0. 01) . 15 patients in the noninvasive group who switched to invasive ventilation were older than those patients continuing noninvasive ventilation.Conclusions For SARS patients fulfilling the ALI/ARDS criteria, the patients underwent noninvasive ventilation are more severe, run a higher probability of developing ARDS from ALI. But earlier initiation of noninvasive ventilation has no impact on mortality. The patients who tolerate noninvasive ventilation can avoid intubation, especially for young patients. However, the time and indication of shifting from noninvasive ventilation to invasive ventilation should be emphasized.