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The critical care management of pleural air leaks can be challenging in all patients, but particularly in patients on mechanical ventilation. To investigate the effect of central airway pressure and pleural pressure on pulmonary air leaks, we studied orotracheally intubated mice with pleural injuries. We used clinically relevant variables - namely, airway pressure and pleural pressure - to investigate flow through peripheral air leaks. The model studied the pleural injuries using a pressure-decay maneuver. The pressure-decay maneuver involved a 3 sec ramp to 30 cmH 2 0 followed by a 3 sec breath hold. After pleural injury, the pressure-decay maneuver demonstrated a distinctive airway pressure time history. Peak inflation was followed by a rapid decrease to a lower plateau phase. The decay phase of the inflation maneuver was influenced by the injury area. The rate of pressure decline with multiple injuries (28 ± 8 cmH 2 0/sec) was significantly greater than a single injury (12 ± 3 cmH 2 O/sec) (P < 0.05). In contrast, the plateau phase pressure was independent of injury surface area, but dependent upon transpulmonary pressure. The mean plateau transpulmonary pressure was 18 ± 0.7 cm H 2 O. Finally, analysis of the inflation ramp demonstrated that nearly all volume loss occurred at the end of inflation (P < 0.001). We conclude that the air flow through peripheral lung injuries was greatest at increased lung volumes and limited by peripheral airway closure. In addition to suggesting an intrinsic mechanism for limiting flow through peripheral air leaks, these findings suggest the utility of positive end-expiratory pressure and negative pleural pressure to maintain lung volumes in patients with pleural injuries., (© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Pleural loculation affects about 30,000 patients annually in the United States and in severe cases can resolve with restrictive lung disease and pleural fibrosis. Pleural mesothelial cells contribute to pleural rind formation by undergoing mesothelial mesenchymal transition (MesoMT), whereby they acquire a profibrotic phenotype characterized by increased expression of α-smooth muscle actin and collagen 1. Components of the fibrinolytic pathway (urokinase plasminogen activator and plasmin) are elaborated in pleural injury and strongly induce MesoMT in vitro. These same stimuli enhance glycogen synthase kinase (GSK)-3β activity through increased phosphorylation of Tyr-216 in pleural mesothelial cells and GSK-3β mobilization from the cytoplasm to the nucleus. GSK-3β down-regulation blocked induction of MesoMT. Likewise, GSK-3β inhibitor 9ING41 blocked induction of MesoMT and reversed established MesoMT. Similar results were demonstrated in a mouse model of Streptococcus pneumoniae-induced empyema. Intraperitoneal administration of 9ING41, after the induction of pleural injury, attenuated injury progression and improved lung function (lung volume and compliance; P < 0.05 compared with untreated and vehicle controls). MesoMT marker α-smooth muscle actin was reduced in 9ING41-treated mice. Pleural thickening was also notably reduced in 9ING41-treated mice (P < 0.05). Collectively, these studies identify GSK-3β as a newly identified target for amelioration of empyema-related pleural fibrosis and provide a strong rationale for further investigation of GSK-3β signaling in the control of MesoMT and pleural injury., (Copyright © 2017 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Effect of time and phosphatidylcholines (PCs) on lubrication of damaged mesothelium has been investigated. Marked increase in coefficient of kinetic friction (μ) of pleural specimens after mesothelial blotting and rewetting decreased by 23.4±3.5%, 41.8±3.8%, and 40.5±2.7% after 30min, 1h, and 2h. Hence, damaged mesothelium is able to partially reset lubricating molecules on its surface. Increase in μ of post-blotting Ringer 2h after addition of unsaturated PCs (3mg/ml) decreased a little more than after 2h Ringer. Effects of unsaturated and saturated PCs were similar, contrary to expectation raised by their different percentage in pleural and alveolar lavage. Effect of PCs did not increase at 6mg/ml, and was nil at 0.4mg/ml. Increase of μ after short phospholipase treatment decreased by 45.9±2.0% after 2h Ringer, and a little more after addition of unsaturated or saturated PCs. Hence, PCs, as other phospholipids, have a small effect, likely because of difficulty in resetting their relationships with main lubricating molecules., (Copyright © 2014 Elsevier B.V. All rights reserved.)

While performing thoracoscopic wedge resection of the lung, the location of the lesion is generally identified by visual inspection or palpation. When difficulty in identification of the lesion by thoracoscopy is anticipated, preoperative marking is performed. However, complications and technical difficulties plague current marking techniques. To overcome this problem, we designed a new, safe and easy marking technique that avoids pleural puncture, called the intrathoracic stamping method.

To determine whether video-assisted thoracoscopic surgery (VATS) is associated with a lower incidence of intrathoracic adhesion after pulmonary resection, we assessed the incidence of adhesion for patients who underwent a second pulmonary resection. The site and extent of adhesion were evaluated by reviewing videotapes recorded during surgery. A significantly (P<0.05) lower rate of mediastinal or interlobar adhesion was observed in patients with pneumothorax (10%) in comparison with lobectomy (57%) or partial resection for tumors (63%), although there were no statistically significant differences in adhesion to the chest wall. There were no significant differences between VATS and thoracotomy for mediastinal or interlobar adhesion. However, a significantly (P<0.05) lower rate of adhesion to the chest wall was observed for VATS (54%) in comparison with thoracotomy (100%). Although VATS resulted in less adhesion to the chest wall than thoracotomy, there was no difference in mediastinal or interlobar adhesion.

Objective: Animal models are indispensable for the development of new therapeutic methods for the closure of alveolar air leakage. However, it is difficult to create a uniform pleural defect model. The purpose of this study was to establish an appropriate animal model for assessing the efficacy and histotoxicity of synthetic sealants for lung surgery., Methods: Nine beagle dogs were used to evaluate the pleural defect model in comparison with conventional resection procedures. A donut-shaped silicon ring with an inner diameter of 15 mm was placed on the pleura, and 0.1 mL of cyanoacrylate was dropped into the ring. A pleural defect was created by sliding a microtome blade just beneath the polymerized cyanoacrylate. Hemostasis was performed by pressure with a sponge., Results: Morphologically, round areas of the pleura were uniformly resected with our procedure. The resected tissue consisted of pleura and thin underlying lung parenchyma. Among the results from 3 surgeons, there were no significant differences in the mean time required for hemostasis (P = .69), the mean thickness of the resected tissue (P = .13), and the mean amount of air leakage from the resected area (P = .19). No penetration of cyanoacrylate into the lung parenchyma was evidenced by immunofluorescence microscopy. Histologically, when the pleura was resected without using cyanoacrylate, a thick fibrocellular layer extended to the lung parenchyma. Furthermore, severe fibrosis was observed when electrocautery was used for hemostasis. However, when the pleura was resected using cyanoacrylate, the normal alveolar structure was preserved., Conclusions: Our uniform pleural defect model using cyanoacrylate may be feasible for the evaluation of synthetic sealants for alveolar air leakage.

The effect of the fibrin adhesive on the gas density of pleura-lung-sutures was investigated in 28 male Wistar rats. Standardized pleura-lung-lacerations were closed by additional fibrin adhesive application in combination with fibrinolytic inhibitors. 30 minutes and 5 days after operation the animals were sacrificed and manometric and micromorphological examinations performed. In good histo-compatibility the additional application of the fibrin adhesive proved to be a proper technique in elevating the pressure tolerance of pleura-lung-sutures significantly.