Is obstructive sleep apnoea associated with hypoxaemia and prolonged ICU stay after type A aortic dissection repair? A retrospective study in Chinese population.

BACKGROUND: Although obstructive sleep apnoea (OSA) is prevalent among patients with aortic dissection, its prognostic impact is not yet determined in patients undergoing major vascular surgery. We aimed to investigate the association of OSA with hypoxaemia and with prolonged intensive care unit (ICU) stay after type A aortic dissection (TAAD) repair. METHODS: This retrospective study continuously enrolled 83 patients who underwent TAAD repair from January 1 to December 31, 2018. OSA was diagnosed by sleep test and defined as an apnoea hypopnea index (AHI) of ≥ 15/h, while an AHI of > 30/h was defined severe OSA. Hypoxaemia was defined as an oxygenation index (OI) of < 200 mmHg. Prolonged ICU stay referred to an ICU stay of > 72 h. Receiver operating characteristic curve analysis was performed to evaluate the predictive value of postoperative OI for prolonged ICU stay. Multivariate logistic regression was performed to assess the association of OSA with hypoxaemia and prolonged ICU stay. RESULTS: A total of 41 (49.4%) patients were diagnosed with OSA using the sleep test. Hypoxaemia occurred postoperatively in 56 patients (67.5%). Postoperatively hypoxaemia developed mostly in patients with OSA (52.4% vs. 83.0%, p = 0.003), and particularly in those with severe OSA (52.4% vs. 90.5%, p = 0.003). The postoperative OI could fairly predict a prolonged ICU stay (area under the receiver-operating characteristic curve, 0.72; 95% confidence intervals [CI] 0.60-0.84; p = 0.002). Severe OSA was associated with both postoperative hypoxaemia (odds ratio [OR] 6.65; 95% CI 1.56-46.26, p = 0.008) and prolonged ICU stay (OR 5.58; 95% CI 1.54-20.24, p = 0.009). CONCLUSIONS: OSA was common in patients with TAAD. Severe OSA was associated with postoperative hypoxaemia and prolonged ICU stay following TAAD repair.

Metatranscriptome of human lung microbial communities in a cohort of mechanically ventilated COVID-19 Omicron patients.

The Omicron variant of the severe acute respiratory syndrome coronavirus 2 (SARS­CoV­2) infected a substantial proportion of Chinese population, and understanding the factors underlying the severity of the disease and fatality is valuable for future prevention and clinical treatment. We recruited 64 patients with invasive ventilation for COVID-19 and performed metatranscriptomic sequencing to profile host transcriptomic profiles, plus viral, bacterial, and fungal content, as well as virulence factors and examined their relationships to 28-day mortality were examined. In addition, the bronchoalveolar lavage fluid (BALF) samples from invasive ventilated hospital/community-acquired pneumonia patients (HAP/CAP) sampled in 2019 were included for comparison. Genomic analysis revealed that all Omicron strains belong to BA.5 and BF.7 sub-lineages, with no difference in 28-day mortality between them. Compared to HAP/CAP cohort, invasive ventilated COVID-19 patients have distinct host transcriptomic and microbial signatures in the lower respiratory tract; and in the COVID-19 non-survivors, we found significantly lower gene expressions in pathways related viral processes and positive regulation of protein localization to plasma membrane, higher abundance of opportunistic pathogens including bacterial Alloprevotella, Caulobacter, Escherichia-Shigella, Ralstonia and fungal Aspergillus sydowii and Penicillium rubens. Correlational analysis further revealed significant associations between host immune responses and microbial compositions, besides synergy within viral, bacterial, and fungal pathogens. Our study presents the relationships of lower respiratory tract microbiome and transcriptome in invasive ventilated COVID-19 patients, providing the basis for future clinical treatment and reduction of fatality.

[Obstructive sleep apnea-hypopnea syndrome in patients with pulmonary thromboembolism: clinical features and management].

OBJECTIVE: To describe the clinical features of obstructive sleep apnea-hypopnea syndrome (OSAHS) in hospitalized pulmonary thromboembolism (PTE) patients, and to explore its impact on the severity of disease and management among patients with PTE. METHODS: Demographic and clinical characteristics of 28 PTE patients complicated with OSAHS admitted to this hospital from January 2002 to December 2010 were analyzed. A total of 30 PTE patients without OSAHS served as a control group. RESULTS: PTE patients with OSAHS had a significantly lower age of onset of disease [(55 ± 11) yr vs (66 ± 11) yr, t = 3.230, P < 0.01], an increased body mass index (BMI) [(30.1 ± 2.8) kg/m(2) vs (26.1 ± 3.1) kg/m(2), t = -4.161, P < 0.001] and a higher smoking index [(19 ± 6) packs/yr vs (8 ± 4) packs/yr, t = -1.713, P < 0.05] when compared with PTE patients without OSAHS. PaO2 [(70 ± 8) mm Hg vs (79 ± 6) mm Hg, 1 mm Hg = 0.133 kPa, t = 4.233, P < 0.05] and involved lung segments [(8 ± 4) vs (5 ± 3), t = -2.496, P < 0.05] in PTE patients with OSAHS were more severe than those in PTE patients without OSAHS. All patients received anticoagulation and/or thrombolysis treatment, and continuous positive airway pressure (CPAP) ventilation was used in some PTE patients with OSAHS. CONCLUSION: PTE patients with OSAHS had a significantly earlier age of onset of disease and more severe conditions than PTE patients without OSAHS. Treatments including anticoagulation and CPAP should be used in these patients.

[Effect of retroviral vector mediating RNA interference on the release of tumor necrosis factor-alpha in lipopolysaccharide-stimulating macrophage].

OBJECTIVE: To explore the effect of small interfering RNA (siRNA) targeting NF-kappaB signal pathway on the expression level of tumor necrosis factor alpha (TNF-alpha) released by lipopolysaccharides (LPS)-stimulating-macrophages. METHODS: Human monocytic THP-1 cell was induced by phorbol myristate acetate (PMA) and transformed into macrophage. Two groups of macrophage were infected by siRNA retroviral expression vector specific to NF-kappaB functional subunit P65 (siRNA group) and Scramble control vector (Scramble control group) constructed by molecular cloning technology. Lipopolysaccharide (50 microg/ml) was used to treat the macrophages continuously. RT-PCR was performed to detect the expression level of NF-kappaB P65 mRNA and TNF-alpha mRNA at different time-points of LPS stimulation. Western blotting was used to analyze the protein level of NF-kappaB P65. Enzyme-linked immunosorbent assay was applied to analyze the expression level of TNF-alpha released by LPS-stimulated macrophages. RESULTS: At Hours 12 and 24 after LPS stimulation, the expression level of NF-kappaB P65 mRNA in siRNA group (0.97 +/- 0.02, 0.89 +/- 0.01) was significantly less than that in Scramble control group (1.01 +/- 0.03, 0.97 +/- 0.01, both P < 0.05). At Hours 24 and 72 after LPS stimulation, the expression level of NF-kappaB P65 protein in siRNA group (0.95 +/- 0.04, 0.94 +/- 0.01) was obviously less than that in Scramble control group (1.07 +/- 0.06, 1.03 +/- 0.05, both P < 0.05). At Hours 4, 8, 12 and 24 after LPS stimulation, TNF-alpha mRNA released by siRNA group macrophages was far less than that by Scramble control group macrophages (0.92 +/- 0.02 vs 0.98 +/- 0.01, 0.86 +/- 0.02 vs 1.00 +/- 0.01, 0.79 +/- 0.03 vs 1.01 +/- 0.01, 0.78 +/- 0.03 vs 1.02 +/- 0.01, all P < 0.05). At Hours 2, 4, 8, 24, 36, 48, 54 and 72 after LPS stimulation, the TNF-alpha content in culture medium supernatant in siRNA group macrophage was less than that in scramble control group (P < 0.05). CONCLUSION: NF-kappaB P65 siRNA inhibits the functional activity of NF-kappaB signal pathway in PMA-induced macrophage. Then it blocks the activation of macrophage and the excessive release of TNF-alpha due to endotoxin stimulation. The RNA interference technology may be applied to prevent and treat excessive inflammatory reaction in acute lung injury.

[Clinical analysis of 62 cases of chronic thromboembolic pulmonary hypertension treated with pulmonary thromboendarterectomy without early and late deaths].

OBJECTIVE: To retrospectively evaluate the effects of pulmonary thromboendarterectomy (PTE) on chronic thromboembolic pulmonary hypertension (CTEPH). METHODS: Sixty-two cases of CTEPH operated with PTE from October 2002 to September 2008 at Anzhen Hospital were retrospectively reviewed and were assigned into either proximal CTEPH group (n = 46) or distal CTEPH group (n = 16). RESULT: No early death was reported. 15 had residual pulmonary hypertension and 23 had pulmonary reperfusion injury postoperatively. And reperfusion injury was recovered with the support of ventilation or ECMO. Between pre and post-procedure, the pulmonary artery systolic pressure changed from 91 +/- 38 mm Hg to 53 +/- 21 mm Hg, the pulmonary vascular resistance from 916 +/- 548 dynxsxcm(-5) to 368 +/- 302 dynxsxcm(-5) (t = 6.896, P = 0.0001), and the arterial partial pressure of oxygen (PaO(2)) from 51 +/- 7 mm Hg to 90 +/- 7 mm Hg and the arterial oxygen saturation (SaO(2)) from 87.0% +/- 3.9% to 96.1% +/- 3.3%, P < 0.05. With the follow-up of (24.8 +/- 14.6) months (cumulative follow-up was 121.6 patient-years), there was no late death and 38 were in NYHA functional class I, 20 class II, 2 class III and 2 class IV. According to Kaplan-Meier actuarial curve, the freedom from reembolism at 3 years was 96.7% +/- 2.8%. The linear bleeding rate related to anticoagulation was 2.47% patient-years, and the linear thromboembolic rate related to anticoagulation is 1.64% patient-years. CONCLUSION: The early and mid-long term survival rate of PTE procedure on CTEPH is acceptable and the complication rate related to anticoagulation with warfarin is relatively low.

[The role of disequilibrium of expression of matrix metalloproteinase-2/9 and their tissue inhibitors in pathogenesis of hyperoxia-induced acute lung injury in mice].

OBJECTIVE: To investigate the role of matrix metalloproteinase-2/9 (MMP-2/9) and their tissue inhibitors (TIMP-1/2) in pathogenesis of acute lung injury (ALI) induced by hyperoxia. METHODS: Seventy-two C57BL/6 mice were randomly divided into normal control group, hyperoxia for 24 hours group, hyperoxia for 48 hours group, and hyperoxia for 72 hours group, with 18 mice in each group. The mice in hyperoxia groups were exposed to >98% oxygen in sealed cages, and the normal control group were placed outside of the cage to breathe room air. At the end of the exposure time the animals were euthanized, the right lung was removed and phosphate buffer solution (PBS) was used to lavage the lung through the endotracheal catheter. The wet/dry weight ratio, broncho-alveolar lavage fluid (BALF) protein content and the volume of pleural fluid were measured, the severity of lung injury was assessed; the expression of MMP-2/9 and TIMP-1/2 mRNA in lung tissue at 24, 48 and 72 hours of hyperoxia were assessed by reverse transcript-polymerase chain reaction (RT-PCR); the amount of MMP-2/9 and TIMP-1/2 protein in lung tissue were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Hyperoxia caused ALI as evidenced by the increase in lung wet/dry weight ratio, BALF protein content and the volume of pleural fluid as compared with the normal control group (P<0.05 or P<0.01). RT-PCR study showed increased expression of MMP-2/9 and TIMP-1 mRNA in lung tissues (P<0.05 or P<0.01), and ELISA assay also demonstrated upregulation of MMP-2/9 and an increase in TIMP-1 amount in BALF compared with their normal control group (P<0.05 or P<0.01). The ratios of both MMP-2 mRNA/TIMP-2 mRNA and MMP-2 protein/TIMP-2 protein were all increased in hyperoxia groups as compared with their normal control group (all P<0.01). CONCLUSION: Hyperoxia causes ALI in mice, and disturbance of MMP-2/TIMP-2 balance plays an important role in the development of hyperoxia-induced ALI in mice.

[The clinical analysis of 54 cases for the surgical treatment of pulmonary embolism].

OBJECTIVE: To evaluate the results of surgical procedures for pulmonary embolism. METHODS: Fifty-four patients of pulmonary embolism received surgical treatment from October 1994 to June 2007, of which 9 were acute pulmonary embolism underwent pulmonary embolectomy and 45 patients were chronic thromboembolic pulmonary hypertension (CTEPH) underwent pulmonary thromboendarterectomy. RESULTS: The mortality rate was 44.4% in acute pulmonary embolism group and 13.3% in CTEPH group (P < 0. 05). Thirteen patients had residual pulmonary hypertension and 23 patients had severe pulmonary reperfusion injury postoperatively. The pulmonary artery systolic pressure changed from (89.4 +/- 36.3) mm Hg (1 mm Hg =0.133 kPa) preoperative to (55.6 +/- 22.4) mm Hg postoperative. The pulmonary vascular resistance changed from (89. 7 +/- 56.7) kPa L(-1) S(-1) preoperative to (38.9 +/- 31.1) kPa L(-1) S(-1) postoperative. The arterial partial pressure of oxygen changed from (52. 3 +/- 6.7 ) mm Hg preoperative to (87.6 +/- 6.5) mm Hg postoperative. The arterial oxygen saturation changed from (88.9 +/- 4.5)% preoperative to (95.3 +/- 2.8 )% postoperative (P < 0.05). With the follow-up of (41.8 +/- 36.4) months, there were 4 patients died. According to NYHA, there were 28 patients for class I , 10 patients for class II and 2 patients for class III. According to Kaplan-Meier survival curve, the 3-year, 4-year, 5-year and 8-year survival rate were (97.1 +/- 2.8 )%, (94.0 +/- 4.1)%, (90.8 +/- 5.2)% and (85.0 +/- 7.3)% respectively. Linear rate of bleeding and thromboembolic related to anticoagulation were 0. 63% patient-years and 0. 62% patient-years respectively. CONCLUSIONS: The operational mortality of acute pulmonary embolism is significantly higher than CTEPH, and the mid-long term survival rate is agreeable and the complication rate related to anticoagulation is relatively low.

[Prognosis of patients with chronic thromboembolic pulmonary hypertension receiving conservative or operative treatments according to a new clinical classification scheme].

OBJECTIVE: To compare the efficacy of conservative or pulmonary thromboendarterectomy (PTE) therapy for chronic thromboembolic pulmonary hypertension (CTEPH) patients according to a new clinical classification scheme. METHODS: This retrospective study analyzed 63 cases of CTEPH admitted to our hospital from February 1995 to October 2007 and 45 cases were treated surgically (Group A) and 18 cases received conservative therapy (Group B). Results were analyzed using Fisher exact test and t test according to San Diego medical center quartering classification scheme and Anzhen Hospital modified bifurcate classification scheme. RESULTS: There were 6 operational deaths in Group A and 2 deaths during hospital stay in Group B. During follow-ups (mean 3.6 +/- 2.5 years), there were 4 deaths in Group A and 9 deaths in Group B. the totality survival rate is significantly higher in Group A than that in Group B (P < 0.05). For patients with San Diego Type I CTEPH, survival rate was significantly higher in Group A compared with Group B (P = 0.009) and was similar for patients with type II and III and IV CTEPH between the two groups (P = 0.338, 0.455, 0.800). Survival rate was significantly higher in Group A than that in Group B for patients with Anzhen central type CTEPH (P = 0.009), but was similar between the two groups for patients with Anzhen peripheral type CTEPH (P = 0.125). The Kaplan-Meier survival curve 5 years survival rate in the Group A was (91.7 +/- 8.0)% for Anzhen central type and (76.0 +/- 8.5)% for Anzhen peripheral type (P = 0.04), and the 5 years Kaplan-Meier survival rate in the Group B was (42.9 +/- 18.7)% for Anzhen central type and (56.2 +/- 10.8)% for Anzhen peripheral type (P = 0.851). CONCLUSION: Anzhen Hospital modified bifurcate classification scheme is a simple and effective classification to predict the prognosis and choose treatment method of CTEPH.

MicroRNA-326 aggravates acute lung injury in septic shock by mediating the NF-κB signaling pathway.

Our previous studies have demonstrated that the activation of the nuclear factor-kappa B (NF-κB) signaling pathway contributes to the development of lipopolysaccharide (LPS)-induced acute lung injury (ALI) as well as an inflammatory reaction, and its inhibition may provide future therapeutic values. Thereby, this study aims to explore the effects of miR-326 on inflammatory response and ALI in mice with septic shock via the NF-κB signaling pathway. The study included normal mice and LPS-induced mouse models of septic shock with ALI. Modeled mice were transfected with the blank plasmid, miR-326 mimic, miR-326 inhibitor, si-BCL2A1 and miR-326 inhibitor + si-BCL2A1. Mean arterial pressure (MAP), airway pressure (AP), heart rate (HR) and lung wet dry (W/D) ratio were determined. Serum levels of interleukin (IL)-6, IL-10, IL-1ß, and tumor necrosis factor-α (TNF-α) were detected using ELISA. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis were performed to detect the miR-326 expression and expression levels of BCL2A1, related genes of inflammatory response and the NF-κB signaling pathway in lung tissues. Cell viability and apoptosis were measured using the CCK-8 assay and flow cytometry, respectively. Compared to the ALI models and those transfected with blank plasmid, the up-regulated miR-326 expression and silenced BCL2A1 lead to decreased levels of MAP, increased AP, HR and lung W/D, increased serum levels of IL-6, IL-10, IL-1ß and TNF-α, increased expressions of IL-6, IL-1ß, TNF-α, NF-κB p65 (p-NF-κB p65), and iNOS with decreased expressions of BCL2A1s as well as inhibition of cell viability and enhanced cell apoptosis; the down-regulated miR-326 expression reversed the aforementioned situation. MiR-326 targeting the BCL2A1 gene activated the NF-κB signaling pathway, resulting in aggravated inflammatory response and lung injury of septic shock with ALI in mice.

Effectiveness and safety of noninvasive positive-pressure ventilation for severe hypercapnic encephalopathy due to acute exacerbation of chronic obstructive pulmonary disease: a prospective case-control study.

BACKGROUND: Although severe encephalopathy has been proposed as a possible contraindication to the use of noninvasive positive-pressure ventilation (NPPV), increasing clinical reports showed it was effective in patients with impaired consciousness and even coma secondary to acute respiratory failure, especially hypercapnic acute respiratory failure (HARF). To further evaluate the effectiveness and safety of NPPV for severe hypercapnic encephalopathy, a prospective case-control study was conducted at a university respiratory intensive care unit (RICU) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) during the past 3 years. METHODS: Forty-three of 68 consecutive AECOPD patients requiring ventilatory support for HARF were divided into 2 groups, which were carefully matched for age, sex, COPD course, tobacco use and previous hospitalization history, according to the severity of encephalopathy, 22 patients with Glasgow coma scale (GCS) < 10 served as group A and 21 with GCS = 10 as group B. RESULTS: Compared with group B, group A had a higher level of baseline arterial partial CO2 pressure ((102 +/- 27) mmHg vs (74 +/- 17) mmHg, P < 0.01), lower levels of GCS (7.5 +/- 1.9 vs 12.2 +/- 1.8, P < 0.01), arterial pH value (7.18 +/- 0.06 vs 7.28 +/- 0.07, P < 0.01) and partial O(2) pressure/fraction of inspired O(2) ratio (168 +/- 39 vs 189 +/- 33, P < 0.05). The NPPV success rate and hospital mortality were 73% (16/22) and 14% (3/22) respectively in group A, which were comparable to those in group B (68% (15/21) and 14% (3/21) respectively, all P > 0.05), but group A needed an average of 7 cm H2O higher of maximal pressure support during NPPV, and 4, 4 and 7 days longer of NPPV time, RICU stay and hospital stay respectively than group B (P < 0.05 or P < 0.01). NPPV therapy failed in 12 patients (6 in each group) because of excessive airway secretions (7 patients), hemodynamic instability (2), worsening of dyspnea and deterioration of gas exchange (2), and gastric content aspiration (1). CONCLUSIONS: Selected patients with severe hypercapnic encephalopathy secondary to HARF can be treated as effectively and safely with NPPV as awake patients with HARF due to AECOPD; a trial of NPPV should be instituted to reduce the need of endotracheal intubation in patients with severe hypercapnic encephalopathy who are otherwise good candidates for NPPV due to AECOPD.

Effects of continuous tracheal gas insufflation during pressure limited ventilation on pulmonary surfactant in rabbits with acute lung injury.

BACKGROUND: Pulmonary surfactant dysfunction may contribute to the development of ventilator induced lung injury (VILI). Tracheal gas insufflation (TGI) is a technique in which fresh gas is introduced into the trachea and augment ventilation by reducing the dead space of ventilatory system, reducing ventilatory pressures and tidal volume (V(T)) while maintaining constant partial arterial CO2 pressure (PaCO(2)). We hypothesised that TGI limited peak inspiratory pressure (PIP) and V(T) and would minimize conventional mechanical ventilation (CMV) induced pulmonary surfactant dysfunction and thereby attenuate VILI in rabbits with acute lung injury (ALI). METHODS: ALI was induced by intratracheal administration of lipopolysaccharide in anaesthetized, ventilated healthy adult rabbits randomly assigned to continuous TGI at 0.5 L/min (TGI group) or CMV group (n = 8 for each group), and subsequently ventilated with limited PIP and V(T) to maintain PaCO(2) within 35 to 45 mmHg for 4 hours. Physiological dead space to V(T) ratio (V(D)/V(T)), dynamic respiratory compliance (Cdyn) and partial arterial O(2) pressure (PaO(2)) were monitored. After ventilation, lungs were analysed for total phospholipids (TPL), total proteins (TP), pulmonary surfactant small to large aggregates ratio (SA/LA) in bronchoalveolar lavage fluid (BALF) and for determination of alveolar volume density (V(V)), myeloperoxidase and interleukin (IL)-8. RESULTS: TGI resulted in significant (P < 0.05 or P < 0.01) decrease in PIP [(22.4 +/- 1.8) cmH2O vs (29.5 +/- 1.1) cmH2O], V(T) [(6.9 +/- 1.3) ml/kg vs (9.8 +/- 1.11) ml/kg], V(D)/V(T) [(32 +/- 5)% vs (46 +/- 2)%], TP [(109 +/- 22) mg/kg vs (187 +/- 25) mg/kg], SA/LA (2.5 +/- 0.4 vs 5.4 +/- 0.7), myeloperoxidase [(6.2 +/- 0.5) U/g tissue vs (12.3 +/- 0.8) U/g tissue] and IL-8 [(987 +/- 106) ng/g tissue vs (24 +/- 3) mN/m] of BALF, and significant (P < 0.05) increase in Cdyn [(0.47 +/- 0.02) ml.cmH2O(-1).kg(-1) vs (0.31 +/- 0.02) ml.cmH2O(-1).kg(-1)], PaO(2) [(175 +/- 24) mmHg vs (135 +/- 26) mmHg], TPL/TP (52 +/- 8 vs 33 +/- 11) and Vv (0.65 +/- 0.05 vs 0.44 +/- 0.07) as compared with CMV. CONCLUSIONS: In this animal model of ALI, TGI decreased ventilatory requirements (PIP, V(T) and V(D)/V(T)), resulted in more favourable alveolar pulmonary surfactant composition and function and less severity of lung injury than CMV. TGI in combination with pressure limited ventilation may be a lung protective strategy for ALI.

Eriodictyol, a plant flavonoid, attenuates LPS-induced acute lung injury through its antioxidative and anti-inflammatory activity.

Acute lung injury (ALI) is characterized by excessive inflammatory responses and oxidative injury in the lung tissue. It has been suggested that anti-inflammatory or antioxidative agents could have therapeutic effects in ALI, and eriodictyol has been reported to exhibit antioxidative and anti-inflammatory activity in vitro. The aim of the present study was to investigate the effect of eriodictyol on lipopolysaccharide (LPS)-induced ALI in a mouse model. The mice were divided into four groups: Phosphate-buffered saline-treated healthy control, LPS-induced ALI, vehicle-treated ALI (LPS + vehicle) and eriodictyol-treated ALI (LPS + eriodictyol). Eriodictyol (30 mg/kg) was administered orally once, 2 days before the induction of ALI. The data showed that eriodictyol pretreatment attenuated LPS-induced ALI through its antioxidative and anti-inflammatory activity. Furthermore, the eriodictyol pretreatment activated the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway in the ALI mouse model, which attenuated the oxidative injury and inhibited the inflammatory cytokine expression in macrophages. In combination, the results of the present study demonstrated that eriodictyol could alleviate the LPS-induced lung injury in mice by regulating the Nrf2 pathway and inhibiting the expression of inflammatory cytokines in macrophages, suggesting that eriodictyol could be used as a potential drug for the treatment of LPS-induced lung injury.

Effect of siRNA against NF-κB on sepsis­induced acute lung injury in a mouse model.

The aim of the present study was to explore the protective effect of small interfering RNA (siRNA) against nuclear factor κB (NF-κB) p65 on sepsis-induced acute lung injury (ALI) in mice. In total, 70 male Kunming mice were randomly divided into a healthy control group, a sepsis group, a specific interfering group and a scrambled control group (Sc), and the latter three groups were divided into post-operational 6 and 12 h subgroups, each of which consisted of 10 mice. The mice were administered with NF-κB siRNA, scrambled siRNA and normal saline via tail vein injection. Following 1 h, a mouse model of septic ALI was produced by cecal ligation and puncture (CLP) in the two siRNA groups and the sepsis control group. At 6 and 12 h post­operation, the experimental mice were sacrificed and the lung tissue samples were collected. Histopathological changes, wet/dry ratio of lung weight, NF-κB protein and NF-κB p65 mRNA levels, matrix metalloproteinase-9 (MMP-9) mRNA and protein activity were detected. Compared with the sepsis group and the Sc at the corresponding time, the expression levels of NF-κB p65 mRNA, the lung injury of experimental mice, the wet/dry ratio and the levels of MMP-9 mRNA and protein activity decreased, and significant differences were observed at 6 h post-operation (P<0.05). RNA interference against NF-κB p65 was able to decrease the expression of NF-κB and further inhibit the early phasic excessive inflammatory reaction in sepsis, which may alleviate ALI.

Efficacy and safety of noninvasive positive pressure ventilation in the treatment of acute respiratory failure after cardiac surgery.

BACKGROUND: Although noninvasive positive pressure ventilation (NPPV) has been successfully used for various kinds of acute respiratory failure, the data are limited regarding its application in postoperative respiratory failure after cardiac surgery. Therefore, we conducted a prospective randomized control study in a university surgical intensive care unit to evaluate the efficacy and safety of NPPV in the treatment of acute respiratory failure after cardiac surgery, and explore the predicting factors of NPPV failure. METHODS: From September 2011 to November 2012 patients with acute respiratory failure after cardiac surgery who had indication for the use of NPPV were randomly divided into a NPPV treatment group (NPPV group) and the conventional treatment group (control group). The between-group differences in the patients' baseline characteristics, re-intubation rate, tracheotomy rate, ventilator associated pneumonia (VAP) incidence, in-hospital mortality, mechanical ventilation time after enrollment (MV time), intensive care unit (ICU) and postoperative hospital stays were compared. The factors that predict NPPV failure were analyzed. RESULTS: During the study period, a total of 139 patients who had acute respiratory failure after cardiac surgery were recorded, and 95 of them met the inclusion criteria, which included 59 males and 36 females with a mean age of (61.5 ± 11.2) years. Forty-three patients underwent coronary artery bypass grafting (CABG), 23 underwent valve surgery, 13 underwent CABG+valve surgery, 13 underwent major vascular surgery, and three underwent other surgeries. The NPPV group had 48 patients and the control group had 47 patients. In the NPPV group, the re-intubation rate was 18.8%, tracheotomy rate was 12.5%, VAP incidence was 0, and the in-hospital mortality was 18.8%, significantly lower than in the control group 80.9%, 29.8%, 17.0% and 38.3% respectively, P < 0.05 or P < 0.01. The MV time and ICU stay (expressed as the median (P25, P75)) were 18.0 (9.2, 35.0) hours and 4.0 (2.0, 5.0) days, which were significantly shorter than in the control group, 96.0 (26.0, 240.0) hours and 6.0 (4.0, 9.0) days respectively, P < 0.05 or P < 0.01. The postoperative hospital stays of the two groups were similar. The univariate analysis showed that the NPPV success subgroup had more patients with acute lung injury (ALI) (17 vs. 0, P = 0.038), fewer patients with pneumonia (2 vs. 7, P < 0.001) and lower acute physiology and chronic health evaluation II (APACHE II) scores (16.1 ± 2.8 vs. 21.8 ± 3.2, P < 0.001). Multivariate analysis showed that pneumonia (P = 0.027) and a high APACHE II score >20 (P = 0.002) were the independent risk factors of NPPV failure. CONCLUSIONS: We conclude that NPPV can be applied in selected patients with acute respiratory failure after cardiac surgery to reduce the need of re-intubation and improve clinical outcome as compared with conventional treatment. Pneumonia and a high APACHE II score >20 might be the independent risk factors of NPPV failure in this group of patients.

Pulmonary oligemia maneuver can alleviate pulmonary artery injury during pulmonary thromboendarterectomy procedure.

BACKGROUND: Pulmonary thromboendarterectomy (PTE) has evolved as a treatment of choice for chronic thromboembolic pulmonary hypertension (CTEPH). This study aimed to characterize if pulmonary oligemia maneuver (POM) can alleviate pulmonary artery injury during PTE procedure. METHODS: A total of 112 cases of CTEPH admitted to Beijing Anzhen Hospital from March 2002 to August 2011 received PTE procedure. They were retrospectively classified as non-POM group (group A, n = 55) or POM group (group B, n = 57). Members from group B received POM during rewarming period, whereas members from group A did not. RESULTS: There were three (5.45%) early deaths in group A, no death in group B (0) (Fisher's exact test, P = 0.118). Six patients in group A needed extracorporeal membrane oxygenation (ECMO) as life support after the PTE procedure, no patients in group B needed ECMO (Fisher's exact test, P = 0.013). The patients in group B had a shorter intubation and ICU stay, lower mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR), higher partial pressure of oxygen in artery (PaO2) and arterial oxygen saturation (SaO2) and less medical expenditure than patients in group A. With a mean follow-up time of (58.3 ± 30.6) months, two patients in group A and one patient in group B died. The difference of the actuarial survival after the procedure between the two groups did not reach statistical significance. Three months post the PTE procedure, the difference of residual occluded pulmonary segment between the two groups did not reach statistical significance (P = 0.393). CONCLUSION: POM can alleviate pulmonary artery injury, shorten ICU stay and intubation time, and lower down the rate of ECMO after PTE procedure.

Osteopontin protects against hyperoxia-induced lung injury by inhibiting nitric oxide synthases.

BACKGROUND: Exposure of adult mice to more than 95% O(2) produces a lethal injury by 72 hours. Nitric oxide synthase (NOS) is thought to contribute to the pathophysiology of murine hyperoxia-induced acute lung injury (ALI). Osteopontin (OPN) is a phosphorylated glycoprotein produced principally by macrophages. OPN inhibits inducible nitric oxide synthase (iNOS), which generates large amounts of nitric oxide production. However, the relationship between nitric oxide and endogenous OPN in lung tissue during hyperoxia-induced ALI has not yet been elucidated, thus we examined the role that OPN plays in the hyperoxia-induced lung injury and its relationships with NOS. METHODS: One hundred and forty-four osteopontin knock-out (KO) mice and their matched wild type background control (WT) were exposed in sealed cages > 95% oxygen or room air for 24- 72 hours, and the severity of lung injury was assessed; expression of OPN, endothelial nitric oxide synthase (eNOS) and iNOS mRNA in lung tissues at 24, 48 and 72 hours of hyperoxia were studied by reverse transcription-polymerase chain reaction (RT-PCR); immunohistochemistry (IHC) was performed for the detection of iNOS, eNOS, and OPN protein in lung tissues. RESULTS: OPN KO mice developed more severe acute lung injury at 72 hours of hyperoxia. The wet/dry weight ratio increased to 6.85 +/- 0.66 in the KO mice at 72 hours of hyperoxia as compared to 5.31 +/- 0.92 in the WT group (P < 0.05). iNOS mRNA (48 hours: 1.04 +/- 0.08 vs. 0.63 +/- 0.09, P < 0.01; 72 hours: 0.89 +/- 0.08 vs. 0.72 +/- 0.09, P < 0.05) and eNOS mRNA (48 hours: 0.62 +/- 0.08 vs. 0.43 +/- 0.09, P < 0.05; 72 hours: 0.67 +/- 0.08 vs. 0.45 +/- 0.09, P < 0.05) expression was more significantly increased in OPN KO mice than their matched WT mice when exposed to hyperoxia. IHC study showed higher expression of iNOS (20.54 +/- 3.18 vs. 12.52 +/- 2.46, P < 0.05) and eNOS (19.83 +/- 5.64 vs. 9.45 +/- 3.82, P < 0.05) in lung tissues of OPN KO mice at 72 hours of hyperoxia. CONCLUSION: OPN can protect against hyperoxia-induced lung injury by inhibiting NOS.

[Prevalence and incidence of deep venous thrombosis among patients in medical intensive care unit].

OBJECTIVE: A cross-sectional study was carried out to observe the prevalence, incidence and risk factors of deep venous thrombosis (DVT) in patients from intensive care unit (ICU). METHODS: Patients who were admitted to respiratory intensive care unit (RICU) and emergency intensive care unit (EICU) of Beijing Chaoyang Hospital and Beijing Anzhen Hospital were screened in our study. All patients enrolled underwent compression ultrasonography (CUS) within 48 h upon their admission to the ICUs. CUS was re-performed at 10 - 14 day, or when leaving ICU or at the time patients developed signs and symptoms (pain, heat, redness, edema) of DVT. Risk factors which were presumed associated with DVT were recorded. The main identified outcome was the presence of DVT. The secondary outcome was pulmonary thromboembolism (PTE). RESULTS: DVT was found in 30 patients of 252 patients within 48 h (11.90%). One hundred seventy-two patients were performed CUS two times or more. 26 patients (15.12%) had DVT. D-dimer, history of operation, kidney failure appeared to be independent risk factors for DVT in ICU patients. 13 patients were suspected PTE and 3 patients diagnosed as PTE. CONCLUSION: ICU doctors should pay more attention to DVT, which is relatively common in ICU patients.