ObjectiveTo explore the value of procalcitonin-to-albumin (PAR) in patients with acute respiratory distress syndrome (ARDS).MethodsA retrospective study was carried on patients diagnosed with ARDS from December 2016 to March 2018. The receiver-operating characteristics (ROC) curve was used to identify the cutoff value of PAR. The association of PAR and 28-day mortality was evaluated using univariate and multivariable Cox regression.ResultsIn the final analysis, there were a total of 255 patients included. Of whom 164 (64.3%) was male, 91 (35.7%) was female and the mean age was 52.1±14.5 years old. The 28-day mortality of all the patients was 32.9% (n=84). ROC curve revealed that the cutoff value of PAR was 0.039 (specificity: 0.714, sensitivity: 0.702) and area under the curve was 0.793 (95%CI: 0.735 - 0.850, P<0.001). The following variables were considered for multivariable adjustment: age, body mass index, pneumonia, aspiration, sepsis, surgery, PaO2/FiO2, red blood cell counts and PAR (P<0.01 in univariate analysis). After multivariable analysis, only age (HR: 1.033, 95%CI: 1.009 - 1.059, P=0.008), PaO2/FiO2 (HR: 0.992, 95%CI: 0.985 - 1.000, P=0.044) and PAR (HR: 4.899, 95%CI: 2.148 - 11.174, P<0.001) remained independently associated with 28-day mortality (P<0.05).ConclusionHigh PAR predicts a poor outcome in ARDS patients, therefore it appears to be a prognostic biomarker of outcomes in patients with ARDS.
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.
ObjectiveTo investigate the role and mechanism of P-selectin glycoprotein ligand-1 (PSGL-1) in hydrochloric acid-induced acute lung injury (ALI) in mice.MethodsWild-type mice (WT) and PSGL-1 knockout mice (PSGL-1 -/-) were randomly subjected to normal saline (NS) or hydrochloric acid (HCl) challenged group. The mice were intratracheally instilled with NS or HCl (1 μl/g weight) into the left lung with a catheter. After 2 hours, respiratory function index enhanced pause (Penh), PaO2 and PaO2 were analyzed. The wet to dry weight ratio (W/D) of the left lung and total protein concentration in bronchoalveolar lavage fluid (BALF) were measured. The number of leukocytes in BALF was counted too. Targeted lung tissue was processed for further HE or immunohistochemistry staining. Meanwhile, the expressions of interleukin-6 (IL-6), IL-1β, nuclear factor-κB (NF-κB), IκBa and p-IκBa in lung tissue were measured.ResultsThe Penh (4.77±1.22 vs. 5.80±0.84) and PaCO2 [(63.7±3.9) mm Hg vs. (74.4±7.4) mm Hg] in the PSGL-1 knockout mice were significantly lower than those in the WT mice after HCl stimulation (P<0.05), while the PaO2 was higher than that in the WT mice [(81.0±7.1) mm Hg vs. (62.0±8.9) mm Hg, P<0.05)]. The lung W/D ratio (4.86±0.15 vs. 5.22±0.20), protein concentration [(3.71±0.64) μg/μl vs. (4.74±0.98) μg/μl] and total leukocyte count [(13.00±2.18) ×107/L vs. (49.42±3.35) ×107/L] in BALF were significantly lower in the PSGL-1 knockout mice challenged with HCl than those in the WT mice (P<0.05). Besides, the protein expressions of IL-6, IL-1β, p65 and p-IκBa in the PSGL-1 knockout mice were lower than those in the WT mice after HCl instillation, while the IκBa expression was higher than that in the WT mice (P<0.05). More numbers of neutrophils and macrophages were found in the lung of the WT mice than the PSGL-1 knockout mice challenged with HCl. However, the differences of above values between the WT mice and the PSGL-1 knockout mice instilled with NS were not found, all of which were significantly lower than the correspongding HCl group except for IκBa (P<0.05).ConclusionPSGL-1 may play important roles in the development of HCl-induced ALI via the NF-κB signaling pathway and inflammation.
ObjectiveTo investigate the effect of ambroxol hydrochloride on c-Jun N-terminal kinase (JNK) signal pathway in gastric aspiration lung injury. MethodsForty healthy male Sprague Dawley rats were randomly divided into a control group, an injury group, a SP600125 (JNK specific inhibitor) group and an ambroxol group. The model of gastric aspiration lung injury was established by aspiration of gastric contents. The rats in the SP600125 group preoperatively received intravenous injection of JNK specific inhibitor SP600125 (3 mg/100 g). The rats in the ambroxol group received intravenous injection of ambroxol hydrochloride (50 mg/kg) 2 hours after the damage occurred. The neutrophil count and malondialdehyde (MDA) activity in bronchoalveolar lavage fluid (BALF), the lung wet weight/dry weight ratio (W/D), and myeloperoxidase (MPO) activity were measured. The protein expressions of JNK and phosphorylated JNK (p-JNK) and inducible nitric oxide synthase (iNOS) in lung tissue were detected by Western blot method. The changes of lung tissue structure were observed under light microscope. ResultsIn the injury group, the neutrophil counts and MDA activity in BALF, W/D, MPO activity, p-JNK and iNOS protein expression increased significantly, lung tissue appeared obvious histopathological injury compared with the control group. In the SP600125 group and the ambroxol group, neutrophil count and MDA activity in BALF, lung W/D, MPO activity, p-JNK and iNOS protein expression were significantly decreased compared with the injury group (P < 0.05), and the damage of the lung tissue pathology was reduced. The expression of JNK protein in lung tissue was not different in all groups (P > 0.05). ConclusionsJNK is involved in inflammatory reaction of gastric aspiration lung injury. The protective effect of ambroxol may be related to the inhibition of JNK signaling pathway and the inhibition of iNOS expression.
ObjectiveTo evaluate the clinical manifestation, radiological, pathological features and treatment of organizing pneumonia (OP) induced by aerosolized recombinant super compound interferon (rSIFN-co). MethodsClinical features and related laboratory examinations of a patient with OP developing after initiation of rSIFN-co for treatment of lung adenocarcinoma were analyzed, and the relevant literature was reviewed. ResultsA 48-year-old man developed cough, fevers, shortness of breath and weight loss, shortly half a month after initiation of therapy with rSIFN-co for lung adenocarcinoma. Chest high resolution computerized tomography (HRCT) showed multiple lung infection diseases. However, the anti-infection treatment was invalid. Lung tissue biopsy by bronchofibroscope was consistent with OP. After discontinuation of rSIFN-co and receiving pulse corticosteroid therapy followed by oral methylprednisolone, the pneumonic symptoms and chest manifestations markedly improved. After eight-month follow-up, the patient's condition was stable. The relative literature screening from Pubmed and Wanfangdata was implemented, but there was no report about OP caused by aerosolized rSIFN-co for lung adenocarcinoma. ConclusionThis report suggests that treatment with aerosolized rSIFN-co for lung adenocarcinoma may induce OP, a rare complication, and clinicians should have vigilance on it.
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.
Objective To establish a rabbit model of ventilator-induced lung injury. Methods Fourty healthy New Zealand rabbits were randomly divided into 3 groups: ie. a routine 8 mL/kg tidal volume group( VT8 group) , 25 mL/kg large tidal volume group( VT25 group) , and 40 mL/kg large tidal volume group( VT40 group) . VT25 and VT40 group were further divided into 2 hours and 4 hours ventilation subgroups. Arterial blood gas, lung mechanical force and hemodynamic parameters were monitored. Lungtissue was sampled for evaluate lung wet/dry ratio and lung injury by HE stain. Bronchoalveolar lavage fluid ( BALF) was collected for measurement of protein concentration, total and differential cell counts. Results Compared with VT8 group, lung injury score in both VT40 and VT25 groups were elevated significantly, ofwhich 4 hour VT40 subgroup was the highest. Lung pathology examination of VT40 group revealed apparent alveolar deformation, interstitial and alveolar space exudation, inflammatory cells infiltration, pulmonary consolidation and alveolar hemorrhage. Lung pathology examination of VT25 group showed pulmonary intervalthickening, inflammatory cells infiltration, while alveolar intravasation was mild. Blood gas analysis showed that PaO2 /FiO2 was deteriorated with time in VT25 and VT40 groups, and PaO2 /FiO2 at the 3 hours in VT40 group( lt; 300 mm Hg) had met the acute lung injury standard, while which in VVT25 group was above 300 mmHg. Lung wet/dry ratio, BALF protein concentration, total nucleated cell and neutrophilic leukocyte were elevated in both VT25 and VT40 groups, of which 4 hours VT40 group was the highest. Conclusion Using 4 hours ventilation at a tidal volume of 40 mL/kg can successfully establish the rabbit model of ventilator-induced lung injury.
Seawater drowning leads to acute lung tissue structure injury, lung ventilation and air exchange dysfunction, acute pulmonary edema, and even acute respiratory failure. The pathogenesis of seawater induced acute lung injury is complex, involving inflammatory response, pulmonary edema, pulmonary surfactant, oxidative stress, apoptosis and autophagy. Timely and effective treatment is the key to reduce the mortality and disability rate of patients with seawater induced acute lung injury. This article summarizes the research progress in the pathogenic mechanism and treatment strategy of seawater induced acute lung injury, aiming to provide reference for the comprehensive treatment of seawater induced acute lung injury patients in clinical work and subsequent related research.
ObjectiveTo assesse the association of an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme gene (ACE) with the risk and the mortality of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). MethodsWe searched electronic databases through April 2014 for the terms "angiotensin-converting enzyme gene", "acute lung injury" and "acute respiratory distress syndrome", and reviewed all studies that reported the relationship of the I/D polymorphism in ACE with ALI/ARDS in adults. Eight studies met the inclusion criteria, comprising 498 ALI/ARDS patients, 3220 healthy controls and 1137 patients without ALI/ARDS. Three genetic models were used: the allele, dominant and recessive models. The meta-analysis was performed with RevMan 5.2 software. ResultsThe ACE I/D polymorphism was not associated with susceptibility to ALI/ARDS compared with the healthy controls and the patient controls for any genetic model. The ACE I/D polymorphism was associated with the mortality risk of ALI/ARDS in Asian subjects, and OR was 2.99 (95% CI 1.87-4.76, P < 0.05), 0.36 (95% CI 0.20-0.67, P < 0.05), 4.62 (95% CI 1.71-12.45, P < 0.05) for allele I/D, genotype II/II+ID and genotype DD/II+ID, respectively. ConclusionThere is a possible association between the ACE I/D polymorphism genotype and the mortality risk of ALI/ARDS in Asians.
Objective To compare three approaches of lipopolysaccharides ( LPS) administration for inducing acute lung injury ( ALI) in mice. Methods LPS ( 5 mg/kg) was intratracheally aerosol administered ( ITA group) , intratracheally instilled ( ITI group) , or intraperitoneally injected ( IPI group) to induce ALI in BLAB/ c mice. Evans Blue instead of LPS was intratracheally administered to observe the liquid distribution in the lungs. Two hours after LPS administration, the mice were sacrificed and the lungs were removed to determine wet-to-dry lung weight ratio ( W/D) , and the histological changes were evaluated by HE staining. Phosphorylation level of IκB-αand NF-κB p65 in lung tissue were investigated by Western blot. Transcription intensity of TNF-α and IL-1β mRNA in lung tissue were detected by real-time quantitative PCR. Results Evans Blue distributed more uniformly in the ITA group than the ITI group. The lung W/D ratio and histological changes score in three LPS administration groups were all significantly higher than the normal control group ( P lt;0. 01) , with the ITA group being the highest. The phosphorylation levels of IκB-αand NF-κB p65 were significantly higher in the ITA group than the ITI group ( P lt;0. 05) , and were significantly higher in the ITI group than the IPI group ( P lt; 0. 05) . Transcription intensity of TNF-αand IL-1βmRNA was significantly higher in the ITA group than the ITI group ( P lt;0. 05) , and were significantly higher in the ITI group than the IPI group ( P lt;0. 05) . Conclusion Being non-invasive and convenient,intratracheal LPS aerosol inhalation is an optimal method to induce ALI in mice because it induces more extensive and uniformly distributed injuries in lung.