Hospital de Clínicas de Porto Alegre Thoracic Surgery Department Ramiro Barcelos, 2350 Largo Eduardo Z. Faraco CEP: 90035-903Porto Alegre , RS - Brazil
Abstract: Lateral thoracic expansion is a surgical technique which consists of increasing the diameter of the thoracic rib cage by the division of ribs and underlying tissue in a staggered fashion. To our knowledge, this procedure has not yet been described in preterm babies. We report a case of a 32-week preterm baby who was initially treated sequentially with resection of the costal cartilages and sternal spreading with the interposition of cartilage grafts, followed by left and right lateral thoracic expansion. The patient survived for 4 months after birth, showing that this procedure can be performed at any age after delivery.
Abstract: Pleural tuberculosis effusion (PTE) in children is a diagnosis which must be considered in isolated pleural effusions in non-toxemic children. It is more common in children over 5 years of age. A history of close contact with an adult with pulmonary tuberculosis reinforces the suspicion for its diagnosis. Pleural effusion without any parenchymal lesion is the characteristic finding on the chest x-ray. However, in 20% to 40% of patients, intrathoracic disease may also occur. Adenosine deaminase, interferon-gamma, analysis of pleural fluid and pleural biopsy are the main tools for diagnostic confirmation. Tuberculin skin test may provide supporting evidence of tuberculous infection. PTE has a good prognosis in children and no long term sequelae are expected.
Abstract: To develop an animal model of diaphragmatic electrical stimulation able to generate an appropriate ventilatory support through the direct implantation of electrodes in the diaphragm (electroventilation).
Abstract: To determine the main congenital lung malformations treated and the principal diagnostic methods employed, as well as the indications for surgical treatment and the results obtained, at a referral facility for pediatric thoracic surgery.
Abstract: To compare the influence of two different ventilation strategies-volume-controlled ventilation (VCV) and pressure-controlled ventilation (PCV)-on the functional performance of lung grafts in a canine model of unilateral left lung transplantation using donor lungs harvested after three hours of normothermic cardiocirculatory arrest under mechanical ventilation.
Abstract: Bronchial carcinoid is an infrequent neoplasm with a neuroendocrine differentiation. Surgical treatment is the gold standard therapy, with procedures varying from sublobar resections to complex lung sparing broncoplastic procedures. This study evaluates the results of surgical treatment of bronchial carcinoids and its prognostic factors.
Abstract: Vascular endothelial growth factor-A (VEGF) is a potent regulator of vascular permeability, inflammatory response, and cell survival in the lung. To explore the functions of VEGF produced locally in type II pneumocytes, we generated mice with a conditional deletion of VEGF-A using Cre recombinase driven by the human surfactant protein C (SPC) promoter. In 7- to 10-week-old VEGF-knockout (SPC-VEGF-KO) mice, lung histology and physiology were essentially normal, except for higher dynamic lung compliance and lower pulmonary vascular permeability. Emphysema was seen in 28- to 32-week-old animals. To investigate the role of type II pneumocyte-derived VEGF in acute lung injury, we challenged 7- to 10-week-old SPC-VEGF-KO mice and their wild-type littermates with intestinal ischemia-reperfusion. Bronchoalveolar lavage fluid total cell count, pulmonary permeability, and lung injury score were significantly attenuated, and total lung VEGF levels were significantly lower in SPC-VEGF-KO mice compared with wild-type controls. In SPC-VEGF-KO mice, activated caspase 3-positive type II epithelial cells were increased after intestinal ischemia-reperfusion, even though there was no significant difference in the total number of cells positive for terminal deoxynucleotidyl transferase dUTP nick-end labeling. We conclude that VEGF in type II cells helps protect alveolar epithelial cells from caspase-dependent apoptosis. However, VEGF produced from type II cells may contribute to increased vascular permeability during acute lung injury.
Abstract: Systemic administration of the low-potassium dextran solution on the peripheral oxidative stress was evaluated in an animal model of lung ischemia-reperfusion in rats. In one experiment, male Wistar rats were divided into two groups (n=5): one received intravenous saline, whereas in the other the animals were given intravenous low potassium dextran solution. In another experiment, male Wistar rats were divided into four groups (n=5): control, ischemia, saline and low potassium dextran. Except for the control animals, all groups were submitted to left hilar clamping for 30 min, followed by reperfusion for 30 min. Saline or low potassium dextran was administered intravenously immediately before clamp removal. In the first experiment there were no significant differences in lipid peroxidation. Total radical trapping potential measurements showed a significant increase in animals receiving low potassium dextran; in the second experiment, there was an increase in lipid peroxidation in both saline and ischemia groups compared to controls, and low potassium dextran. Low potassium dextran group showed an increase in total radical trapping potential measurements compared to all other groups. Ischemia-reperfusion injury mediated by reactive oxygen species was attenuated by the systemic use of low potassium dextran in this animal model of ischemia-reperfusion of the lung.
Abstract: The overproduction of reactive oxygen species plays an important role in the cascade of events during lung ischemia-reperfusion leading to graft failure. An evaluation of the peripheral markers of oxidative stress and antioxidant enzyme activities was carried out after reperfusion in a rat lung transplant model. The decrease in lipid peroxidation immediately after transplantation ( P < 0.05) may suggest an adaptative response and/or a protective effect of low potassium dextran against lipid peroxidation through natural scavenging mechanisms.
Abstract: OBJECTIVE: To evaluate the effect of lung ischemic preconditioning (IPC) on normothermic ischemia/reperfusion (I/R) injury in a rat model, quantifying the production of reactive oxygen species. METHODS: Forty-seven male Wistar rats were randomized into four groups: control, sham, I/R and IPC. Control group animals were anesthetized and killed by decapitation, after which pneumonectomy was performed and the left lungs were stored in liquid nitrogen. Sham, IPC and I/R group rats were anesthetized, tracheostomized, ventilated, anticoagulated and submitted to left thoracotomy with dissection of the left pulmonary artery for clamping. Sham group rats underwent dissection of the left pulmonary artery, I/R group rats underwent 30 min of total hilar clamping, and IPC group rats underwent 5-min clamping of the left pulmonary artery followed by 30 min of total hilar clamping. Lungs were reperfused for 90 min and ventilated with the same parameters, with additional positive end-expiratory pressure of 1 cmH2O. Hemodynamic and blood gas values were obtained prior to thoracotomy, prior to total hilar clamping, after 30 min of reperfusion and after 90 min of reperfusion. Lipid peroxidation was determined by measuring levels of thiobarbituric acid reactive substances. RESULTS: There were no significant differences among the groups in terms of the levels of thiobarbituric acid reactive substances. Nor were there any significant differences among the sham, I/R and IPC groups in terms of arterial oxygen tension, arterial carbon dioxide tension or hemodynamic values. CONCLUSIONS: In an in situ I/R rat model, 5-min IPC of the left pulmonary artery does not attenuate I/R injury.
Abstract: OBJECTIVE: To assess the esophageal function profile and the prevalence of gastro-esophageal reflux (GER) in lung transplant candidates. METHODS: From July of 2005 to November of 2006, a prospective study was conducted involving 55 candidates for lung transplantation at the Santa Casa de Misericórdia Hospital in Porto Alegre, Brazil. Prior to transplantation, patients underwent outpatient stationary esophageal manometry and 24-h esophageal pH-metry using one and two electrodes. RESULTS: Abnormal esophageal manometry was documented in 80% of the patients, and 24% of the patients presented pathological acid reflux. Digestive symptoms presented sensitivity and specificity for GER of 50% and 61%, respectively. Of the patients with chronic obstructive pulmonary disease, 94% presented abnormal esophageal manometry, and 80% presented lower esophageal sphincter hypotonia, making it the most common finding. Patients with bronchiectasis presented the highest prevalence of GER (50%). CONCLUSIONS: In patients with advanced lung disease, GER is highly prevalent. In the population studied, digestive symptoms of GER were not predictive of pathological acid reflux. The role that GER plays in chronic rejection should be examined and clarified in future studies.
Abstract: OBJECTIVE: To evaluate post-operative complications in living lobar lung transplant donors. METHODS: Between September of 1999 and May of 2005, lobectomies were performed in 32 healthy lung transplant donors for 16 recipients. The medical charts of these donors were retrospectively analyzed in order to determine the incidence of postoperative complications and alterations in pulmonary function after lobectomy. RESULTS: Twenty-two donors (68.75%) presented no complications. Among the 10 donors presenting complications, the most frequently observed complication was pleural effusion, which occurred in 5 donors (15.6% of the sample). Red blood cell transfusion was necessary in 3 donors (9.3%), and 2 donors underwent a second surgical procedure due to hemothorax. One donor presented pneumothorax after chest tube removal, and one developed respiratory infection. There were two intra-operative complications (6.25%): one donor required bronchoplasty of the middle lobe; and another required lingular resection. No intra-operative mortality was observed. Post-operative pulmonary function tests demonstrated an average reduction of 20% in forced expiratory volume in one second (p < 000.1) compared to pre-operative values. CONCLUSIONS: Lobectomy in living lung transplant donors presents high risk of post-operative complications and irreversible impairment of pulmonary function. Careful pre-operative evaluation is necessary in order to reduce the incidence of complications in living lobar lung transplant donors.
Abstract: PURPOSE: To evaluate the effects of alveolar recruitment based on mean airway pressure (MAP) on pig lungs submitted to thoracotomy through blood gas exchange and hemodynamic parameters. METHODS: Twelve pigs weighting approximately 25 Kg were intubated and ventilated on volume controlled ventilation (tidal volume 10 ml/Kg, respiratory rate 16 min, FiO2 1.0, inspiratory:expiratory ratio 1:2, PEEP 5 cmH2O). The animals were then randomized into two groups: control and left lateral thoracotomy. The PEEP was increased at each 15-minute intervals to reach a MAP of 15, 20 and 25 cmH2O, respectively. Hemodynamic, gas exchange and respiratory mechanic data were measured immediately before each PEEP change. RESULTS: There were no significant differences between both groups in all parameters analyzed (P=1.0). The PaO2, PaCO2, MAP, PAP and plateau pressure were significantly worse at MAP of 25 cmH2O, when compared with the other values of MAP (P=0.001, P=0.039, P=0.001, P=0.016 e P=0.027, respectively). The best pulmonary performance according to the analyzed parameters was observed at MAP of 20 cmH2O. CONCLUSION: PEEP adjusted to MAP of 20 cmH2O resulted in best arterial oxygenation, without compromising the venous return, as opposed to MAP of 25 cmH2O, which caused deterioration of gas exchange, hemodynamics and respiratory mechanic.
Abstract: AIM: The aim of this article was to determine sentinel lymph node (SLN) identification rate (IR) using Patent Blue V in patients with non-small cell lung cancer (NSCLC) and to evaluate the accuracy of SLN for the presence of mediastinal metastasis. METHODS: Between 2004 and 2006 the data from 32 patients with clinical stage IA to IIB, who underwent lung resection for NSCLC, were prospectively analyzed. Patent blue V dye was injected in the peritumoral tissue, and the first lymph node to stain was identified as a sentinel node. RESULTS: SLN was identified in fifteen patients (IR=46.9%). SLN with metastatic involvement was observed in four patients. Accuracy, sensitivity and specificity of the sentinel lymph node in predicting the status of other mediastinal lymph node stations were respectively 86.7%, 100%, and 84.6%. In 63.1% patients, the SLNs corresponded to the lymph node stations 10 and 11. In seven patients (36.9%), the SLNs were located in the N2 stations. CONCLUSION: Although the use of Patent Blue V for SLN identification is feasible, this technique presents relatively low identification rate. The major difficulty on the detection of SLNs was the black coloration of the lymph node, which interfered with the visualization of the dye.
Abstract: The increasing demand in transplantation research requires efficient and less expensive animal models in order to obtain reliable results that are reproducible in larger animal models and, ultimately, applied clinically. The model of unilateral left lung transplantation in rats has proven to be a useful alternative for those purposes. We demonstrate a technical modification of this model, which consists of the isolation and ligation of the contralateral (right) pulmonary artery, allowing blood circulation exclusively in the transplanted lung. This model is feasible and reproducible. However, the short survival time restricts the assessment of the transplanted lung to a maximum period of three hours.
Abstract: Most acute respiratory distress syndrome studies have been focused on the lung injury. Little is known about other organs during the development of acute respiratory distress syndrome. Herein, we investigated the injury and cell death in multiple organs after intestinal ischemia-reperfusion (IIR) in C57BL/6 mice. Terminal transferase dUTP nick end labeling staining was used as a marker of cell death. Caspase 3 and cathepsin B activation as markers of caspase-dependent and caspase-independent apoptosis, respectively, and electron microscopy for ultimate characterization of cell death were used. In comparison with control and sham-operated mice, the IIR group showed interstitial inflammatory infiltrates in the lung and significant increases of lung injury parameters and plasma lactate dehydrogenase and aspartate aminotransferase levels. Terminal transferase dUTP nick end labeling-positive cells and immunostaining for hemeoxygenase 1, an enzyme induced by inflammatory stimuli, were increased in the lung, heart, and kidney, but not in the liver. The number of hemeoxygenase 1-positive cells positively and significantly correlated to the number of terminal transferase dUTP nick end labeling-positive cells. Cell death was not associated with caspase 3 or cathepsin B activation. Electron microscopy showed morphological features compatible with oncotic rather than apoptotic cell death or necrosis, including mitochondrial swelling and cytoplasm disorganization in pulmonary and renal epithelial cells, lung and cardiac endothelial cells, and myocytes. These results indicate that, although lung injury is the most significant manifestation after IIR, oncotic cell death occurs in the lung, heart, and kidney, which may be related to ischemia and inflammation.
Abstract: Emphysema is a chronic lung disease characterized by alveolar enlargement and tissue loss. Tissue engineering represents an attractive potential for regeneration of several organ systems. The complex three-dimensional architectural structure of lung parenchyma requiring connections of alveolar units to airways and the pulmonary circulation makes this strategy less optimistic. In the present study, we used Gelfoam sponge as a scaffold material, supplemented with fetal rat lung cells as progenitors, to explore the potential application of cell-based tissue engineering for lung regeneration in adult rats. After injection into lung parenchyma, the sponge showed porous structures similar to alveolar units. It did not induce severe local inflammatory response. Fetal lung cells in the sponge were able to survive in the adult lung for at least 35 days, determined by CMTMR [5-(and-6)-{[(4-chloromethyl)benzoyl]amino}tetramethylrhodamine] labeling. Proliferation of cells within the sponge was demonstrated in vivo by bromodeoxyuridine (BrdU) labeling. Cells formed "alveolar-like structures" at the border between the sponge and the surrounding lung tissue with positive immunohistochemical staining for epithelial and endothelial cells. Neovascularization of the sponge was demonstrated with India ink perfusion. The sponge degraded after several months. This study suggests that cell-based tissue engineering possesses the potential to regenerate alveolar-like structures, an important step towards our ultimate goal of lung regeneration.
Abstract: INTRODUCTION: The function of the vascular endothelial growth factor (VEGF) system in acute lung injury (ALI) is controversial. We hypothesized that the role of VEGF in ALI may depend upon the stages of pathogenesis of ALI. METHODS: To determine the responses of VEGF and its receptors during the early onset of ALI, C57BL6 mice were subjected to intestinal ischemia or sham operation for 30 minutes followed by intestinal ischemia-reperfusion (IIR) for four hours under low tidal volume ventilation with 100% oxygen. The severity of lung injury, expression of VEGF and its receptors were assessed. To further determine the role of VEGF and its type I receptor in lung epithelial cell survival, human lung epithelial A549 cells were treated with small interference RNA (siRNA) to selectively silence related genes. RESULTS: IIR-induced ALI featured interstitial inflammation, enhancement of pulmonary vascular permeability, increase of total cells and neutrophils in the bronchoalveolar lavage (BAL), and alveolar epithelial cell death. In the BAL, VEGF was significantly increased in both sham and IIR groups, while the VEGF and VEGF receptor (VEGFR)-1 in the lung tissues were significantly reduced in these two groups. The increase of VEGF in the BAL was correlated with the total protein concentration and cell count. Significant negative correlations were observed between the number of VEGF or VEGFR-1 positive cells, and epithelial cells undergoing cell death. When human lung epithelial A549 cells were pre-treated with 50 nM of siRNA either against VEGF or VEGFR-1 for 24 hours, reduced VEGF and VEGFR-1 levels were associated with reduced cell viability. CONCLUSION: These results suggest that VEGF may have dual roles in ALI: early release of VEGF may increase pulmonary vascular permeability; reduced expression of VEGF and VEGFR-1 in lung tissue may contribute to the death of alveolar epithelial cells.
Abstract: BACKGROUND: Innate immunity is the first line of host defense against invading microorganisms, which is mediated by specific pathogen recognition molecules called toll-like receptors (TLRs). TLRs can also recognize endogenous "danger" signals, resulting in cytokine production and activation of the adaptive immune system. We hypothesized that gene expression of TLRs during lung transplantation may be affected by the donor condition and the ischemia-reperfusion process, which may subsequently influence graft function. METHODS: Lung biopsies from 14 patients were collected before and after reperfusion, and mRNA levels of TLRs, cytokines (interleukin [IL]-1beta, IL-6, IL-8, IL-10 and interferon-gamma) and heat-shock protein 70 (HSP70) were measured by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: In cold-preserved donor lungs, all TLRs (except TLR3) showed significant correlations with one another and also with the cytokines examined. Expression of several TLRs and cytokines correlated with the intubation time of donors. TLR4 gene expression correlated closely with IL-8 before and after reperfusion (p </= 0.01). After reperfusion, HSP70 mRNAs increased significantly (p < 0.05). CONCLUSIONS: Differential expression levels of TLRs and cytokine genes likely reflect the inflammatory status of lung grafts; correlation of TLR genes with cytokine genes and clinical conditions implicates a potential role of TLRs in early graft responses.
Abstract: OBJECTIVE: To analyze the impact that comorbidities have on the postoperative outcomes in patients submitted to lobectomy for the treatment of bronchial carcinoma. METHODS: A retrospective study of 493 patients submitted to lobectomy for the treatment of bronchial carcinoma was conducted, and 305 of those patients met the criteria for inclusion in the final study sample. The surgical technique used was similar in all cases. The Torrington-Henderson scale and the Charlson scale were used to analyze comorbidities and to categorize patients into groups based on degree of risk for postoperative complications or death. RESULTS: The postoperative (30-day) mortality rate was 2.9%, and the postoperative complications index was 44%. Prolonged air leakage was the most common complication (in 20.6%). The univariate analysis revealed that gender, age, smoking, neoadjuvant therapy and diabetes all had a significant impact on the incidence of complications. The factors found to be predictive of complications were body mass index (23.8 +/- 4.4), forced expiratory volume in one second (74.1 +/- 24%) and the ratio between forced expiratory volume in one second and forced vital capacity (0.65 +/- 0.1). The scales employed proved efficacious in the identification of the risk groups, as well as in drawing correlations with morbidity and mortality (p = 0.001 and p < 0.001). In the multivariate analysis, body mass index and the Charlson index were found to be the principal determinants of complications. In addition, prolonged air leakage was found to be the principal factor involved in mortality (p = 0.01). CONCLUSION: Reductions in forced expiratory volume in one second, in the ratio between forced expiratory volume in one second and forced vital capacity, and in body mass index, as well as a Charlson score of 3 or 4 and a Torrington-Henderson score of 3, were associated with a greater number of postoperative complications in patients submitted to lobectomy for the treatment of bronchial carcinoma. Air leakage was found to be strongly associated with mortality.
Abstract: Long pentraxin 3 (PTX3), an acute-phase protein, is a newly clarified mediator for innate immunity and inflammation. As a soluble pattern recognition receptor, it has a nonredundant role in antifungal infection. Overexpression of PTX3 worsens acute lung injury. The lung epithelium is a critical factor in defense against pulmonary pathogens; it is also involved in acute inflammatory responses related to tissue injury. However, very little is known about how PTX3 is regulated in the lung epithelium. In this study, we found that i.v. injection of LPS induced PTX3 expression in rat lung alveolar epithelium. Using human lung cell lines and primary epithelial cells, we found that PTX3 expression was significantly up-regulated by TNF-alpha in a time- and dose-dependent manner, but not by LPS. Pretreatment with either actinomycin D or cycloheximide abolished TNF-alpha-induced PTX3 expression, indicating the requirement for both transcriptional and translational regulation. The TNF-alpha-induced PTX3 expression was blocked by SP600125, a JNK-specific inhibitor, but not by the inhibitors against NF-kappaB, ERKs, or p38 MAPK. Knockdown of either JNK1 or JNK2 with small interfering RNA also significantly reduced the regulated PTX3 expression. Thus, lung epithelial cells appear to be a major local source for PTX3 production, which could be induced in vivo from these cells by LPS or other inflammatory stimuli, and may be an important mediator for host defense and tissue damage. The importance of the JNK pathway for the regulated PTX3 expression may be a potential target for its regulation in the lung.
Abstract: Traditionally, the recognition and tolerance of transplanted grafts has been considered to be within the realm of the adaptive immune system. Innate immunity, on the other hand, as the first line of host defense, plays a role in fighting against invading microorganisms. Recently, with the discovery of the Toll-like receptors (TLRs), the role of innate immune responses in the control of adaptive immunity has become a new area of interest. Emerging evidence suggests that in addition to responding to pathogen-associated molecular patterns of microorganisms, TLRs can be activated by endogenous ligands, expressed by mammalian cells. These 'danger signals' may participate in ischemia-reperfusion related organ damage and subsequently influence function and survival of transplanted grafts. Furthermore, it has been suggested that adaptive immune responses can enhance the acute inflammatory responses controlled by innate immunity in organ transplantation. This review addresses the potential involvement of TLRs in different stages of organ transplantation. Intriguing and controversial findings are presented and discussed in order to stimulate more attention to this emerging and potentially important area of research in organ transplantation.
Abstract: Cdx-2 is a transactivator for the proglucagon gene in pancreatic and intestinal endocrine cells. Cdx-2 is also expressed in differentiated intestinal epithelia of nonendocrine origin. Cdx-2-/- mice are embryonic lethal, while Cdx-2+/- mutants show multiple malfunctions including the formation of intestinal polyps. Within the polyps, the remaining wild type Cdx-2 allele ceases its expression, while the expression of both Cdx-2 and proglucagon in the endocrine cells remains unaltered, indicating that Cdx-2 could be haplo-insufficient for nonendocrine cells, but not for proglucagon producing endocrine cells. We propose that mechanisms underlying Cdx-2 expression and auto-regulation [Xu F, Li H & Jin T (1999), J Biol Chem274, 34310-34316] differ in these two types of cells. We show here that forskolin and cAMP upregulate Cdx-2 expression in proglucagon producing cells, but not in colon cancer cells and primary intestinal cell cultures. It is unlikely that the activation is mainly mediated by PKA, because the activation was observed in a PKA deficient cell line. Co-transfecting a dominant negative Ras expression plasmid substantially repressed the Cdx-2 promoter, in contrast to a previous finding that Ras is a negative factor for Cdx-2 expression in colon cancer cells. Furthermore, forskolin activated ERK1/2 phosphorylation in the endocrine cells, and attenuation of ERK1/2 phosphorylation by its inhibitor is associated with attenuated Cdx-2 expression. Finally, an Epac pathway specific cAMP analogue stimulated both ERK1/2 phosphorylation and Cdx-2 expression. Taken together, our observations suggest that Cdx-2 expression is regulated by the second messenger cAMP, cell-type specifically, via the Epac pathway.
Abstract: We present a novel animal model for post-transplant obliterative airway disease in which the donor trachea is implanted into the recipient's lung parenchyma. Although this procedure is technically more challenging than the heterotopic model of implantation into a subcutaneous pouch, it has several important advantages some of which are the appropriate local environment and the possibility of local immunosuppressive therapy after transtracheal gene, cell or drug delivery. This model has revealed new insights into angiogenic potential of the pulmonary circulation.
Abstract: BACKGROUND: The purpose of this study was to evaluate canine lungs obtained from non-heart-beating donors after unilateral lung transplantation subjected to partial liquid ventilation with perfluorodecalin. METHODS: Twelve donor dogs were killed and kept under mechanical ventilation for 3 hours. Heart-lung blocks were harvested after retrograde pulmonary hypothermic flush with Perfadex. Left lung grafts were randomly transplanted into 12 weight-matched recipient animals. Animals were divided into 2 groups: control (standard mechanical ventilation, n = 6) and PLV (partial liquid ventilation, n = 6). Forty-five minutes after transplantation, the animals in the PLV group received perfluorodecalin (15 ml/kg) via orotracheal tube. All animals received volume-controlled ventilation (FIO2) 1.0, PEEP 5 cm H(2)O) over 6 consecutive hours. Thereafter, blood-gas analysis, ventilatory mechanics and hemodynamics were registered at 30-minute intervals. After 6 hours of reperfusion the animals were killed and the transplanted lungs were extracted to obtain the wet/dry weight ratio. RESULTS: There were significant differences in pulmonary arterial pressure, which were higher in control group animals (p < 0.009). The control animals also showed higher arterial PaO(2) than those in the PLV group (p < 0.00001), but lower PaCO(2) (p < 0.008). The peak and plateau pressures were higher in the PLV group (p < 0.00001). Neither static compliance nor wet/dry weight ratios were different in between groups. CONCLUSIONS: PLV with perfluorodecalin yields functional results compatible with life in this model. Nonetheless, pulmonary gas exchange and mechanics were superior after reperfusion in animals given conventional mechanical ventilation up to 6 hours after left lung allotransplantation.
Abstract: Recent evidence suggests that alveolar epithelial cells (AECs) may contribute to the development, propagation, and resolution of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Proinflammatory cytokines, pathogen products, and injurious mechanical ventilation are important contributors of excessive inflammatory responses in the lung. In the present study, we used cDNA microarrays to define the gene expression patterns of A549 cells (an AEC line) in the early stages of three models of pulmonary parenchymal cell activation: cells treated with tumor necrosis factor-alpha (TNFalpha) (20 ng/ml), lipopolysaccharide (LPS, 1 microg/ml), or cyclic stretch (20% elongation) for either 1 h or 4 h. Differential gene expression profiles were determined by gene array analysis. TNFalpha induced an inflammatory response pattern, including induction of genes for chemokines, inflammatory mediators, and cell surface membrane proteins. TNFalpha also increased genes related to pro- and anti-apoptotic proteins, signal transduction proteins, and transcriptional factors. TNFalpha further induced a group of genes that may form a negative feedback loop to silence the NFkappaB pathway. Stimulation of AECs with mechanical stretch changed cell morphology and activated Src protein tyrosine kinase. The combination of TNFalpha plus stretch enhanced or attenuated expression of multiple genes. LPS decreased microfilament polymerization but had less impact on NFkappaB translocation and gene expression. Results from this study indicate that AECs can tailor their response to different stimuli or/and combination of stimuli and subsequently play an important role in acute inflammatory responses in the lung.
Abstract: Aortopulmonary paraganglioma is a rare tumor of the mediastinum. The only effective treatment is complete resection, which may pose a surgical challenge because of its proximity to the heart, great vessels, and trachea, often rendering a complete resection difficult to achieve. We report a case in which the tumor was excised under cardiopulmonary bypass and resulted in massive bleeding only controlled by means of packing the pleural cavity during 48 hours, known as damage control strategy. The patient survived and has been disease-free for 2 years.
