Although mechanical ventilation is an important therapy, it can result in complications. One major complication is ventilator-induced lung injury, which is caused by alveolar hyperdistension, leading to an inflammatory process, with neutrophilic infiltration, hyaline membrane formation, fibrogenesis and impaired gas exchange. In this process, cellular mechanotransduction of the overstretching stimulus is mediated by means of the cytoskeleton and its cell-cell and cell-extracellular matrix interactions, in such a way that the mechanical stimulus of ventilation is translated into an intracellular biochemical signal, inducing endothelial activation, pulmonary vascular permeability, leukocyte chemotaxis, cytokine production and, possibly, distal organ failure. Clinical studies have shown the relationship between pulmonary distension and mortality in patients with ventilator-induced lung injury. However, although the cytoskeleton plays a fundamental role in the pathogenesis of ventilator-induced lung injury, there have been few in vivo studies of alterations in the cytoskeleton and in cytoskeleton-associated proteins during this pathological process.

Keywords: Respiration, artificial; Cytoskeleton; Cell adhesion molecules; Focal adhesions; Mechanotransduction, cellular

Objective: To evaluate the effects that pulmonary resection has on pulmonary function and quality of life (QoL) in patients with primary or metastatic lung cancer. Methods: This was a prospective cohort study involving all patients submitted to pulmonary resection for cancer between September of 2006 and March of 2007 at the A. C. Camargo Hospital in São Paulo, Brazil. Patients underwent spirometry in the preoperative period and at six months after the surgical procedure. After a postoperative period of six months, the patients completed an overall QoL questionnaire (the Medical Outcomes Study 36-item Short-form Health Survey) and another one, specific for respiratory symptoms (the Saint George's Respiratory Questionnaire). The scores obtained in our study were compared with those previously obtained for a general population and for a population of patients with COPD. Results: We included 33 patients (14 males and 19 females), ranging in age from 39 to 79 years. All of the patients, smokers and nonsmokers alike, presented significant worsening of pulmonary function. The mean scores on the overall QoL questionnaire were approximately 5% lower than those obtained for the general population. The scores of various domains of the symptom-specific QoL questionnaire were 50-60% lower than those obtained for the general population and approximately 20% higher than those obtained for the population with COPD. Conclusions: Pulmonary resection has a direct negative impact on pulmonary function and QoL, especially on the QoL related to aspects directly linked to pulmonary function. We highlight the importance of preoperative assessment of pulmonary function in patients undergoing pulmonary resection, in order to predict their postoperative evolution.

Keywords: Thoracic surgery; Lung neoplasms/surgery; Spirometry; Quality of life; Questionnaires.

Acute respiratory distress syndrome (ARDS) is characterized by diffuse alveolar damage, and evolves progressively with three phases: exsudative, fibroproliferative, and fibrotic. In the exudative phase, there are interstitial and alveolar edemas with hyaline membrane. The fibroproliferative phase is characterized by exudate organization and fibroelastogenesis. There is proliferation of type II pneumocytes to cover the damaged epithelial surface, followed by differentiation into type I pneumocytes. The fibroproliferative phase starts early, and its severity is related to the patient's prognosis. The alterations observed in the phenotype of the pulmonary parenchyma cells steer the tissue remodeling towards either progressive fibrosis or the restoration of normal alveolar architecture. The fibrotic phase is characterized by abnormal and excessive deposition of extracellular matrix proteins, mainly collagen. The dynamic control of collagen deposition and degradation is regulated by metalloproteinases and their tissular regulators. The deposition of proteoglycans in the extracellular matrix of ARDS patients needs better study. The regulation of extracellular matrix remodeling, in normal conditions or in several pulmonary diseases, such as ARDS, results from a complex mechanism that integrate the transcription of elements that destroy the matrix protein and produce activation/inhibition of several cellular types of lung tissue. This review article will analyze the ECM organization in ARDS, the different pulmonary parenchyma remodeling mechanisms, and the role of cytokines in the regulation of the different matrix components during the remodeling process.

Keywords: Respiratory distress syndrome. Pulmonary alveoli/lesions. Extracellular matrix. Cytokines/ultrastructure.