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To investigate the long-term efficacy of percutaneous transluminal pulmonary angioplasty (PTPA) in patients with Takayasu arteritis (TA) and pulmonary artery stenosis and pulmonary hypertension (PH). Data from 183 lesions from 79 surgeries performed on 32 patients with TA and PH were analyzed. Symptoms, laboratory investigation results, World Health Organization (WHO) functional class, 6-min walk distance (6 MWD), hemodynamic parameters, and prognosis were analyzed at baseline and follow-up. The mean (± SD) age of the 32 patients (28 female, 4 male) was 42.8 ± 11.9 years, and the median follow-up was 49.5 months (interquartile range, 26-71 months). Compared with baseline, changes in total bilirubin, N-terminal pro-brain natriuretic peptide (NT-proBNP) level, 6 MWD, and WHO score functional class demonstrated significant differences ( <0.001). Echocardiography findings, right and left ventricular diameter, tricuspid annular plane systolic excursion, and estimated pulmonary artery systolic pressure were all improved ( =0.016, <0.001, <0.001, =0.005, respectively). Importantly, repeat right heart catheterization revealed that mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac index also improved significantly at follow-up ( <0.001, <0.001, and =0.011, respectively). Pulmonary angiography revealed post-procedure restenosis in 64 (35.0%) lesions underwent PTPA within three to six months. Among three patients who underwent stent implantation, one experienced restenosis. Two patients died during the follow-up period, one from aggravation of right heart failure after lung infection, and the other in a traffic accident. Results of this study indicated that PTPA significantly improved clinical symptoms, exercise tolerance, and hemodynamic parameters in patients with TA pulmonary artery stenosis and PH. More importantly, reperfusion pulmonary edema significantly decreased, and no patient died of PTPA-related complications with guidance from the pressure wire.

Reperfusion pulmonary edema (RPE) is a severe complication after pulmonary endarterectomy (PEA) and is associated with prolonged mechanical ventilation, organ dysfunction, and worse outcome. While residual pulmonary hypertension after PEA is associated with RPE, studies on preoperative risk factors for RPE after PEA are scarce. We investigated a potential association between preoperative hemodynamic values and development of RPE after PEA surgery. All adult CTEPH‐patients who underwent PEA surgery at the Kerckhoff‐Clinic Bad Nauheim, Germany, between 2018 and 2021 were included. The primary endpoint was development of postoperative RPE. Preoperative hemodynamic values and patient characteristics were compared between patients with and without RPE. Receiver Operating Characteristic curve analysis and logistic regression models were used for identification of risk factors for RPE. A total of 483 patients were included in this analysis (mean age 61 ± 13 years, 57% male). 75 patients developed postoperative RPE. ROC analysis revealed a significant discrimination for RPE by preoperative mean pulmonary artery pressure (mPAP) [AUC = 0.7, 95% CI: 0.622–0.779]. According to the Youden Index, the cut‐off for preoperative mPAP was 54.5 mmHg. Multivariable logistic regression identified preoperative mPAP [OR: 2.684 95% CI: 1.220–5.904, p = 0.014] as independent risk factor for development of RPE after PEA surgery. Our study determines preoperative mPAP value as an independent risk factor for development of RPE after PEA surgery. These results might help to identify patients with an increased risk for RPE and adapt perioperative therapy accordingly.

Primary graft dysfunction, a form of reperfusion pulmonary edema that occurs early after lung transplantation, shares key clinical and pathological features with acute lung injury and its more severe form, the acute respiratory distress syndrome. However, in contrast to acute lung injury/acute respiratory distress syndrome, in which biomarkers in plasma, urine and lung edema fluid have prognostic and pathogenetic value, the role of biomarkers in primary graft dysfunction has been less thoroughly explored. This review summarizes human and animal studies on biomarkers in primary graft dysfunction, including cytokines and markers of acute inflammation, VEGF, endothelial markers and adhesion molecules, markers of coagulation and fibrinolysis and markers of lung epithelial injury. Similarities to the literature in acute lung injury/acute respiratory distress syndrome are highlighted where appropriate, and future directions for research on the role of biomarkers in primary graft dysfunction are suggested.

Diaphragmatic hernia (DH) can be a result of congenital or acquired causes. Congenital hernias that have been reported in veterinary medicine are pleuroperitoneal, peritoneal pericardial, and hiatal. Trauma is the most common cause of acquired DH. Traumatic DH is classified as either acute or chronic, depending on the time from the initial injury. The most common clinical signs of patients presenting with DH are related to the respiratory and/or gastrointestinal tracts. A complete history, thorough physical exam, and diagnostic imaging are required for an accurate diagnosis. Patient stabilization is paramount for debilitated patients in respiratory distress and/or shock from trauma. Emergency surgical intervention is recommended for patients refractory to stabilization efforts.

The management of massive pulmonary embolism remains difficult, particularly when cardiogenic shock is involved. In an attempt to rescue and maintain the preoperative circulatory condition, seven patients with acute pulmonary embolism were given percutaneous cardiopulmonary support (PCPS). The circulation, respiratory condition, and urinary output were all improved after PCPS induction. Two patients died of profound cardiogenic shock before the operation. Five patients underwent surgical embolectomy. Postoperatively, all patients who underwent embolectomy were continuously assisted with PCPS. The overall survival rate after PCPS induction was 42.9% (3/7), and the success rate of surgical embolectomy was 60% (3/5). One of the major complications associated with PCPS was bleeding, which can be associated with preoperative thrombolysis. The use of PCPS immediately resuscitated and stabilized the hemodynamic condition and allowed a successful emergency pulmonary embolectomy to be performed. Additionally, PCPS was effective for postoperative respiratory management, which is sometimes associated with reperfusion pulmonary edema.[PUBLICATION ABSTRACT]

Ischemia-reperfusion (IR)-induced acute lung injury (ALI) is implicated in several clinical conditions including lung transplantation, cardiopulmonary bypass surgery, re-expansion of collapsed lung from pneumothorax or pleural effusion and etc. IR-induced ALI remains a challenge in the current treatment. Carbonic anhydrase has important physiological function and influences on transport of CO2. Some investigators suggest that CO2 influences lung injury. Therefore, carbonic anhydrase should have the role in ALI. This study was undertaken to define the effect of a carbonic anhydrase inhibitor, acetazolamide (AZA), in IR-induced ALI, that was conducted in a rat model of isolated-perfused lung with 30 minutes of ischemia and 90 minutes of reperfusion. The animals were divided into six groups (n = 6 per group): sham, sham + AZA 200 mg/kg body weight (BW), IR, IR + AZA 100 mg/kg BW, IR + AZA 200 mg/kg BW and IR+ AZA 400 mg/kg BW. IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, pulmonary hypertension, neutrophilic sequestration, and an increase in the expression of pro-inflammatory cytokines. Increases in carbonic anhydrase expression and perfusate pCO2 levels were noted, while decreased Na-K-ATPase expression was noted after IR. Administration of 200mg/kg BW and 400mg/kg BW AZA significantly suppressed the expression of pro-inflammatory cytokines (TNF-α, IL-1, IL-6 and IL-17) and attenuated IR-induced lung injury, represented by decreases in pulmonary hyper-permeability, pulmonary edema, pulmonary hypertension and neutrophilic sequestration. AZA attenuated IR-induced lung injury, associated with decreases in carbonic anhydrase expression and pCO2 levels, as well as restoration of Na-K-ATPase expression.

Lung ischemia-reperfusion injury (LIRI) causes oxidative stress, inflammation, and immune system activation. The Nrf2/Keap1/HO-1 pathway is important in cellular defense against these effects. Quercetin, a flavonoid with antioxidant, anti-inflammatory, and anti-cancer properties, has been investigated. Our aim in this study was to investigate the effect of quercetin on preventing lung ischemia-reperfusion injury and the role of the Nrf2/Keap1/HO-1 pathway. Sixty-four male Wistar rats were divided into four distinct groups( n  = 16). Sham, lung ischemia-reperfusion (LIR), Saline + LIR, Quercetin + LIR (30 mg/kg i.p for a week before LIR). LIR groups were subjected to 60 min of ischemia (left pulmonary artery, vein, and bronchus) and 120 min of reperfusion. Our assessment encompassed a comprehensive analysis of various factors, including the evaluation of expression Nrf2, Keap1, and Heme Oxygenase-1 (HO-1) levels and NF-κB protein. Furthermore, we examined markers related to inflammation (interleukin-1β and tumor necrosis factor alpha), oxidative stress (malondialdehyde, total oxidant status, superoxide dismutase, glutathione peroxidase, total antioxidant capacity), lung edema (Wet/dry lung weight ratio and total protein concentration), apoptosis (Bax and Bcl2 protein), and histopathological alterations (intra-alveolar edema, alveolar hemorrhage, and neutrophil infiltration). Our results show that ischemia-reperfusion results in heightened inflammation, oxidative stress, apoptosis, lung edema, and histopathological damage. Quercetin showed preventive effects by reducing these markers, acting through modulation of the Nrf2/Keap1 pathway and inhibiting the NF-κB pathway. This anti-inflammatory effect, complementary to the antioxidant effects of quercetin, provides a multifaceted approach to cell protection that is important for developing therapeutic strategies against ischemia-reperfusion injury and could be helpful in preventive strategies against ischemia-reperfusion.

Hypoxia preconditioning has been proven to be an effective method to enhance the therapeutic action of mesenchymal stem cells (MSCs). However, the beneficial effects of hypoxic MSCs in ischemia/reperfusion (I/R) lung injury have yet to be investigated. In this study, we hypothesized that the administration of hypoxic MSCs would have a positive therapeutic impact on I/R lung injury at molecular, cellular, and functional levels. I/R lung injury was induced in isolated and perfused rat lungs. Hypoxic MSCs were administered in perfusate at a low (2.5×105 cells) and high (1×106 cells) dose. Rats ventilated with a low tidal volume of 6 ml/kg served as controls. Hemodynamics, lung injury indices, inflammatory responses and activation of apoptotic pathways were determined. I/R induced permeability pulmonary edema with capillary leakage and increased levels of reactive oxygen species (ROS), pro-inflammatory cytokines, adhesion molecules, cytosolic cytochrome C, and activated MAPK, NF-κB, and apoptotic pathways. The administration of a low dose of hypoxic MSCs effectively attenuated I/R pathologic lung injury score by inhibiting inflammatory responses associated with the generation of ROS and anti-apoptosis effect, however this effect was not observed with a high dose of hypoxic MSCs. Mechanistically, a low dose of hypoxic MSCs down-regulated P38 MAPK and NF-κB signaling but upregulated glutathione, prostaglandin E2, IL-10, mitochondrial cytochrome C and Bcl-2. MSCs infused at a low dose migrated into interstitial and alveolar spaces and bronchial trees, while MSCs infused at a high dose aggregated in the microcirculation and induced pulmonary embolism. Hypoxic MSCs can quickly migrate into extravascular lung tissue and adhere to other inflammatory or structure cells and attenuate I/R lung injury through anti-oxidant, anti-inflammatory and anti-apoptotic mechanisms. However, the dose of MSCs needs to be optimized to prevent pulmonary embolism and thrombosis.

Axl is a cell surface receptor tyrosine kinase, and activation of the Axl attenuates inflammation induced by various stimuli. Growth arrest-specific 6 (Gas6) has high affinity for Axl receptor. The role of Gas6/Axl signaling in ischemia-reperfusion-induced acute lung injury (IR-ALI) has not been explored previously. We hypothesized that Gas6/Axl signaling regulates IR-induced alveolar inflammation via a pathway mediated by suppressor of cytokine signaling 3 (SOCS3). IR-ALI was induced by producing 30 min of ischemia followed by 90 min of reperfusion in situ in an isolated and perfused rat lung model. The rats were randomly allotted to a control group and IR groups, which were treated with three different doses of Gas6. Mouse alveolar epithelium MLE-12 cells were cultured in control and hypoxia-reoxygenation (HR) conditions with or without Gas6 and Axl inhibitor R428 pretreatment. We found that Gas6 attenuated IR-induced lung edema, the production of proinflammatory cytokines in perfusates, and the severity of ALI ex vivo. IR down-regulated SOCS3 expression and up-regulated NF-κB, and Gas6 restored this process. In the model of MLE-12 cells with HR, Gas6 suppressed the activation of TRAF6 and NF-κB by up-regulating SOCS3. Axl expression of alveolar epithelium was suppressed in IR-ALI but Gas6 restored phosphorylation of Axl. The anti-inflammatory effect of Gas6 was antagonized by R428, which highlighted that phosphorylation of Axl mediated the protective role of Gas6 in IR-ALI. Gas6 up-regulates phosphorylation of Axl on alveolar epithelium in IR-ALI. The Gas6/Axl signaling activates the SOCS3-mediated pathway and attenuates IR-related inflammation and injury.

Chronic thromboembolic pulmonary hypertension (CTEPH) can be treated with pulmonary thromboendarterectomy (PTE) which may lead to reperfusion lung injury (RPLI) and postoperative pneumonia. We aimed to describe the incidence, diagnostic characteristics, and clinical outcomes of post-PTE pneumonia compared to RPLI. A retrospective study involving CTEPH subjects who underwent PTE at a large referral center was conducted. Data included demographics, hemodynamics, microbiologic diagnostics, and clinical outcomes. Post-PTE pneumonia was diagnosed based on documentation, signs/symptoms, or microbiologic sampling within seven days of surgery. Among 75 PTE subjects, 21 (28%) had RPLI, and 18 (24%) had post-PTE pneumonia. Of those with RPLI, 48% had pneumonia, suggesting overlap. Eight of 75 (11%) subjects underwent bronchoscopic sampling, and five (63%) samples yielded positive results indicative of infection. Subjects with post-PTE pneumonia and RPLI had longer hospital and ICU lengths of stay and mechanical ventilation duration than either group alone. Post-PTE pneumonia is prevalent and overlaps with RPLI in CTEPH subjects. The study highlights the importance of systematic evaluation and early detection of pneumonia in subjects with RPLI post-PTE. Timely diagnosis and management of pneumonia may improve outcomes. Further research is needed to understand risk factors and develop preventive strategies for post-PTE pneumonia.