Objective: To investigate the effects of N-acetylcysteine (NAC) and pentoxifylline in a model of remote organ injury after hind-limb ischemia/reperfusion (I/R) in rats, the lungs being the remote organ system. Methods: Thirty-five male Wistar rats were assigned to one of five conditions (n = 7/group), as follows: sham operation (control group); hind-limb ischemia, induced by clamping the left femoral artery, for 2 h, followed by 24 h of reperfusion (I/R group); and hind-limb ischemia, as above, followed by intraperitoneal injection (prior to reperfusion) of 150 mg/kg of NAC (I/R+NAC group), 40 mg/kg of pentoxifylline (I/R+PTX group), or both (I/R+NAC+PTX group). At the end of the trial, lung tissues were removed for histological analysis and assessment of oxidative stress. Results: In comparison with the rats in the other groups, those in the I/R group showed lower superoxide dismutase activity and glutathione levels, together with higher malondialdehyde levels and lung injury scores (p < 0.05 for all). Interstitial inflammatory cell infiltration of the lungs was also markedly greater in the I/R group than in the other groups. In addition, I/R group rats showed various signs of interstitial edema and hemorrhage. In the I/R+NAC, I/R+PTX, and I/R+NAC+PTX groups, superoxide dismutase activity, glutathione levels, malondialdehyde levels, and lung injury scores were preserved (p < 0.05 for all). The differences between the administration of NAC or pentoxifylline alone and the administration of the two together were not significant for any of those parameters (p > 0.05 for all). Conclusions: Our results suggest that NAC and pentoxifylline both protect lung tissue from the effects of skeletal muscle I/R. However, their combined use does not appear to increase the level of that protection.

Keywords: Skeletal muscle; Ischemia; Reperfusion injury; Lung injury; Acetylcysteine; Pentoxifylline.

Background: It is questionable whether pressure-controlled ventilation (PCV) has advantages over volume-cycled ventilation (VCV). Objectives: To compare PCV to VCV with decelerating flow profile during assisted and controlled modes in an acute lung injury experimental model. Methods: Severe acute lung injury (PaO2/FIO2 < 100 mmHg) was induced by oleic acid IV infusion (0.05 mg/kg) in seven dogs. The animals were submitted to PCV and VCV in a randomized sequence. After 40 minutes in the assisted mode, ventilation was changed to the controlled mode after neuromuscular blockade. The tidal volume and the inspiratory time were kept constant throughout the experiment. Results: There were no differences in gas exchange (PaO2 and PaCO2), cardiac output or oxygen delivery (DO2) between VCV and PCV. The same was observed regarding maximum airway and plateau pressures, and also to the static compliance. Oxygen consumption (VO2) after neuromuscular blockade was 124 ± 48 in VCV versus 143 ± 50 ml/min in PCV, p = 0.42. In the assisted mode, there was a statistical trend of a higher VO2 in PCV (219 ± 72 versus 154 ± 67 ml/min in VCV, p = 0.06), that was associated with a statistical trend of a higher oxygen cost of breathing (OCB) during assisted PCV, although without statistical significance (31 ± 77 in VCV versus 75 ± 96 ml/min in PCV, p = 0.23), and also in a lower PvO2 (34 ± 7 in PCV versus 42 ± 6 ml/min in VCV, p = 0.02). These occurred despite a higher maximum inspiratory flow in the assisted mode in PCV (58 ± 9 versus 48 ± 4 L/min in VCV, p = 0.01). In both VCV and PCV the institution of controlled ventilation reduced cardiac debit and DO2 in as much as 20% relative to the assisted mode. Conclusions: The implementation of controlled ventilation improved the oxygen delivery/consumption relationship in this severe and with high OCB acute lung injury model. The PCV offered no additional benefits to VCV and it was associated with a higher OCB during the assisted mode.

Keywords: Artificial respiration. Pulmonary gas exchange. Tidal volume.

Objective: To determine whether tramadol has a protective effect against lung injury induced by skeletal muscle ischemia-reperfusion. Methods: Twenty Wistar male rats were allocated to one of two groups: ischemia-reperfusion (IR) and ischemia-reperfusion + tramadol (IR+T). The animals were anesthetized with intramuscular injections of ketamine and xylazine (50 mg/kg and 10 mg/kg, respectively). All of the animals underwent 2-h ischemia by occlusion of the femoral artery and 24-h reperfusion. Prior to the occlusion of the femoral artery, 250 IU heparin were administered via the jugular vein in order to prevent clotting. The rats in the IR+T group were treated with tramadol (20 mg/kg i.v.) immediately before reperfusion. After the reperfusion period, the animals were euthanized with pentobarbital (300 mg/kg i.p.), the lungs were carefully removed, and specimens were properly prepared for histopathological and biochemical studies. Results: Myeloperoxidase activity and nitric oxide levels were significantly higher in the IR group than in the IR+T group (p = 0.001 for both). Histological abnormalities, such as intra-alveolar edema, intra-alveolar hemorrhage, and neutrophil infiltration, were significantly more common in the IR group than in the IR+T group. Conclusions: On the basis of our histological and biochemical findings, we conclude that tramadol prevents lung tissue injury after skeletal muscle ischemia-reperfusion.

Keywords: Tramadol; Muscle, skeletal; Ischemic attack, transient; Lung Injury.

Objective: To investigate the effects of quercetin in a model of bleomycin-induced pulmonary inflammation and fibrosis. Methods: Seventynine adult male hamsters were randomized to receive intratracheal (IT) instillations and intraperitoneal (IP) injections in four configurations: IP vehicle/IT saline (VS group, n = 16); IP quercetin/IT saline (QS group, n = 16); IP vehicle/IT bleomycin (VB group, n = 27); and IP quercetin/ IT bleomycin (QB group, n = 20). Quercetin and bleomycin were administered at 30 mg/kg/day and 10 U/kg, respectively. Quercetin was started/discontinued 3 days before/14 days after the IT instillations. Results: The mortality rate was significantly higher in the VB group than in the other groups (44% vs. VS: 0%; QS: 0%; and QB: 15%). Lung levels of thiobarbituric acid reactive substances (× 10−2 nmol/mg) were significantly higher in the VB group (6.6 ± 1.3 vs. VS: 5.5 ± 0.8; QS: 2.5 ± 0.6; and QB: 5.8 ± 0.6). Lung levels of reduced glutathione (× 10−2 nmol/mg) were significantly lower in the VB/QB groups than in the VS/QS groups (28.9 ± 13.8/28.6 ± 14.8 vs. 43.9 ± 16.0/51.1 ± 20.3), whereas those of hydroxyproline (mg/g) were significantly higher (201.6 ± 37.3/177.6 ± 20.3 vs. 109.6 ± 26.1/117.5 ± 32.0).Mean lung septal thickness (μm) was greatest in the VB group (16.9 ± 3.2 vs. VS: 3.0 ± 0.3; QS: 3.3 ± 0.2; and QB: 5.2 ± 1.1). Conclusions: In a hamster model of lung injury, quercetin exhibited anti-inflammatory effects that are related, at least in part, to its antioxidant properties.

Keywords: Pulmonary fibrosis; Bleomycin; Flavonoids; Lipid peroxidation.

Objective: To evaluate the effects of azathioprine on the mucociliary system in a model of bronchial section and anastomosis in rats. Methods: Thirty-six male Wistar-Furth rats were submitted to left bronchial section and anastomosis and divided into two groups to receive either saline solution or azathioprine. After 7, 15 and 30 days of treatment, six animals from each group were killed, after which in situ mucociliary transport velocity, in vitro mucus transportability, and contact angle of mucus in the right (intact) and left (sectioned) bronchi were measured. Results: In situ mucociliary transport velocity was significantly lower in the sectioned bronchi than in the intact bronchi (p < 0.001). In situ mucociliary transport velocity was lower in the intact bronchi of the animals treated with azathioprine for 7 days (p < 0.05), and those bronchi presented full recovery after 30 days of treatment. The contact angle was higher in the mucus samples collected from the sectioned bronchi of the animals treated with saline solution for 30 days (p < 0.001), which is in accordance with the decreased in vitro mucus transportability observed in the same animals (p < 0.001). Conclusions: We conclude that, in the sectioned bronchi of rats, treatment with azathioprine causes only transitory impairment of mucociliary transport, whereas administration of saline solution impairs mucociliary transport for up to 30 days. In addition, azathioprine protects against alterations in mucus surface properties.

Keywords: Mucociliary clearance; Anastomosis, surgical; Immunosuppression; Lung.

Objective: To evaluate structural alterations of the lung in rats with diabetes mellitus (DM), by quantifying oxidative stress and DNA damage, as well as to determine the effects that exogenous superoxide dismutase (SOD) has on such alterations. Methods: A controlled experimental study involving 40 male Wistar rats, divided into four groups (10 animals each): control; SOD-only (without DM but treated with SOD); IDM-only (with streptozotocin-induced DM but untreated); and IDM+SOD (with streptozotocin-induced DM, treated with SOD). The animals were evaluated over a 60-day period, day 0 being defined as the day on which the streptozotocin-injected animals presented glycemia > 250 mg/dL. The SOD was administered for the last 7 days of that period. At the end of the study period, samples of lung tissue were collected for histopathological analysis, evaluation of tissue oxidative stress, and assessment of DNA damage. Results: There were no significant differences among the groups regarding DNA damage. In the IDM-only group, there was a significant increase in the extracellular matrix and significantly greater hyperplasia of the capillary endothelium than in the SOD-only and control groups. In addition, there were significant changes in type II pneumocytes and macrophages, suggesting an inflammatory process, in the IDM-only group. However, in the IDM+SOD group, there was a reduction in the extracellular matrix, as well as normalization of the capillary endothelium and of the type II pneumocytes. Conclusions: Exogenous SOD can reverse changes in the lungs of animals with induced DM.

Keywords: Diabetes mellitus, experimental; Oxidative stress; Lung; DNA damage.

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 compare the effects that prone and supine positioning during high-frequency oscillatory ventilation (HFOV) have on oxygenation and lung inflammation, histological injury, and oxidative stress in a rabbit model of acute lung injury (ALI). Methods: Thirty male Norfolk white rabbits were induced to ALI by tracheal saline lavage (30 mL/kg, 38°C). The injury was induced during conventional mechanical ventilation, and ALI was considered confirmed when a PaO2/FiO2 ratio < 100 mmHg was reached. Rabbits were randomly divided into two groups: HFOV in the supine position (SP group, n = 15); and HFOV with prone positioning (PP group, n = 15). For HFOV, the mean airway pressure was initially set at 16 cmH2O. At 30, 60, and 90 min after the start of the HFOV protocol, the mean airway pressure was reduced to 14, 12, and 10 cmH2O, respectively. At 120 min, the animals were returned to or remained in the supine position for an extra 30 min. We evaluated oxygenation indices and histological lung injury scores, as well as TNF-α levels in BAL fluid and lung tissue. Results: After ALI induction, all of the animals showed significant hypoxemia, decreased respiratory system compliance, decreased oxygenation, and increased mean airway pressure in comparison with the baseline values. There were no statistically significant differences between the two groups, at any of the time points evaluated, in terms of the PaO2 or oxygenation index. However, TNF-α levels in BAL fluid were significantly lower in the PP group than in the SP group, as were histological lung injury scores. Conclusions: Prone positioning appears to attenuate inflammatory and histological lung injury during HFOV in rabbits with ALI.

Keywords: Respiration, artificial/adverse effects; Prone position; Lung/physiopathology; Pneumonia; Respiratory distress syndrome, adult; Acute lung injury; Disease models, animal; Rabbits.

Objective: This study aimed to investigate acute and chronic effects of varenicline on lung tissue in an experimental study. Methods: A total of 34 rats were randomly allocated into study (varenicline) and control groups. The rats were divided into two groups (i) control group, (ii) varenicline group. Then, the rats in the each group were sub‑divided equally in turn as acute (C1; V1) and chronic (C2; V2) ; all rats of acute and chronic groups were sacrificed under the anesthesia on the 45th day for acute group [C1 (n=5) and V1 (n=12)] and the 90th day for chronic group [C2 (n=5) and V2 (n=12)], respectively. Thus, biochemical and histopathological analysis were carried out. Results: Thirty four rats completed the study, 24 were in varenicline group and 10 were in control group. In chronic exposure to varenicline, oxidant levels comprising of malondialdehyde (MDA), and myeloperoxidase (MPO) increased and superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) levels, named as antioxidants, decreased significantly when compared to the control group. MDA and MPO levels were also significantly higher and SOD, CAT, GPx, GSH levels were also significantly lower in chronic varenicline group when compared to acute varenicline group. These findings were also supported by histopathological observations. Conclusion: This is the first study, which evaluated pulmonary effects of varenicline experimentally on an animal model. It was observed that chronic varenicline treatments cause inflammation and lung cell injury.

Keywords: Varenicline; Lung tissue; Oxidative stress; Pulmonary toxicity.

Objective: To evaluate the effects of immunization with a DNA-hsp65 vaccine in an experimental model of pulmonary fibrosis. Methods: A total of 120 male C57BL/6 mice were distributed into four groups: SS, injected with saline (placebo) and then receiving intratracheal (IT) instillation of saline; SB, injected with saline (placebo) and then receiving IT instillation of bleomycin; PB, treated with plasmid only, without bacterial genome, and then receiving IT instillation of bleomycin; and BB, treated with the vaccine and then receiving IT instillation of bleomycin. Bleomycin was instilled 15 days after the last immunization, and the animals were killed six weeks thereafter. The left and right lungs were removed, the former for morphological analysis and the latter for hydroxyproline measurements. Results: The proportion of deaths within the first 48 h after the IT instillation (deaths attributed to the surgical procedure) was higher in the SB group than in the SS group (57.7% vs. 11.1%). The mean area of pulmonary interstitial septa was greater in the SB and PB groups (53.1 ± 8.6% and 53.6 ± 9.3%, respectively) than in the SS and BB groups (32.9 ± 2.7% and 34.3 ± 6.1%, respectively). The mean area of interstitial septa stained by picrosirius was greater in the SB, PB and BB groups than in the SS group (8.2 ± 4.9%, 7.2 ± 4.2% and 6.6 ± 4.1%, respectively, vs. 2.0 ± 1.4%). The total hydroxyproline content in the lung was significantly lower in the SS group (104.9 ± 20.9 pg/lung) than in the other groups (SB: 160.4 ± 47.8 pg/lung; PB: 170.0 ± 72.0 pg/lung; and BB: 162.5 ± 39.7 pg/lung). Conclusions: Immunization with the DNA-hsp65 vaccine reduced the deposition of noncollagen matrix in a model of bleomycin-induced lung lesion.

Keywords: Pulmonary fibrosis; Bleomycin; Collagen.

Objective: To evaluate the stability of hemodynamic, respiratory and gas exchange variables in an animal model of oleic acid-induced acute lung injury. Methods: This was an experimental study involving 10 mongrel dogs. The variables were measured at baseline, as well as at 30, 60, 90 and 120 min after the administration of oleic acid. In order to analyze repeated measurements, linear and quadratic effects were tested. Mixed linear models with diversified variance and covariance structures were used, depending on the variable studied. Results: We found that mean arterial blood pressure stabilized at 30 min, as did heart rate, pulmonary arterial pressure and pulmonary capillary pressure at 60 min. Respiratory rate, tidal volume, minute volume and respiratory work stabilized at 30 min. Regarding gas exchange variables, PaO2, PaO2/FiO2 ratio and pulmonary shunt fraction stabilized at 30 min. The remaining variables maintained a continuous rise or fall. Conclusions: This oleic acid-induced acute lung injury model is stable for some of the variables tested, although stabilization occurs at different times. The respiratory and gas exchange variables stabilized at 30 min, whereas the hemodynamic variables stabilized at 60 min.

Keywords: Respiratory distress syndrome, adult; Models, animal; Statistical analysis.

Objective: To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs. Methods: Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water. Results: The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former. Conclusions: Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels.

Keywords: Lung; Methylprednisolone; Glucocorticoids; Lipid peroxidation; Antioxidant response elements.

Objective: To study the effects of short-term exposure to high oxygen concentrations (hyperoxia) on Wistar rat lungs. Methods: Animals were divided into three groups exposed to hyperoxia for 10', 30' and 90' (O10', O30', O90', respectively), together with a control group (exposed to room air). The animals were sacrificed 24 h after exposure. Bronchoalveolar lavage was performed, and the lungs were removed for histological and stereological analysis. Results: In the O10', O30', and O90' groups, respectively and in comparison with the controls, we observed an increase in the numbers of macrophages (2169.9 ± 118.0, 1560.5 ± 107.0, and 1467.6 ± 39.0 vs. 781.3 ± 78.3) and neutrophils (396.3 ± 35.4, 338.4 ± 17.3, and 388.7 ± 11.7 vs. 61.6 ± 4.2), concomitant with an increase in oxidative damage (143.0 ± 7.8%, 180.4 ± 5.6%, and 235.0 ± 13.7% vs. 100.6 ± 1.7%). The histological and stereological analyses revealed normal alveoli and alveolar septa in the controls (83.51 ± 1.20% and 15 ± 1.21%), in the O10' group (81.32 ± 0.51% and 16.64 ± 0.70%), and in the O30' group (78.75 ± 0.54% and 17.73 ± 0.26%). However, in the O90' group, inflammatory cell infiltration was observed in the alveoli and alveolar septa. Red blood cells extravasated from capillaries to the alveoli (59.06 ± 1.22%), with evidence of congestion, hemorrhage, and septal edema (35.15 ± 0.69%). Conclusion: Hyperoxia for 90' caused injury of the lung parenchyma, resulting in oxidative damage and inflammatory cell infiltration.

Keywords: Hyperoxia; Lung/injuries; Oxidative stress.

Objective: Brain death (BD) triggers important hemodynamic and inflammatory alterations, compromising the viability of organs suitable for transplantation. To better understand the mi-crocirculatory alterations in donor lungs caused by BD. The present study investigated the pul-monary microcirculation in a rodent model of BD via intravital microscopy. Methods: Male Wistar rats were anaesthetized and mechanically ventilated. They were trepanned and BD was induced through the increase in intracranial pressure. As control group, sham-operated (SH) rats were trepanned only. In both groups, expiratory O2 and CO2 were monitored and after three hours, a thoracotomy was performed, and a window was created to observe the lung surface using an epi-fluorescence intravital microscopy. Lung expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) was evaluated by immunohistochemistry, and cytokines were measured in lung samples. Results: Three hours after the surgical proce-dures, pulmonary perfusion was 73% in the SH group. On the other hand, BD animals showed an important decrease in organ perfusion to 28% (p = 0.036). Lung microcirculatory compromise after BD induction was associated with an augmentation of the number of leukocytes recruited to lung tissue, and with a reduction in eNOS expression and an increase in ICAM-1 expression on lung endothelial cells. BD rats showed higher values of expiratory O2 and lower values of CO2 in comparison with SH animals after three hours of monitoring. Conclusion: Data presented showed that BD triggers an important hypoperfusion and inflammation in the lungs, compromis-ing the donor pulmonary microcirculation

Keywords: Brain death; Inflammation; Intravital microscopy; Lung microcirculation.

Background: Lung volume reduction surgery may be a viable treatment alternative for emphysema patients suffering from severe respiratory insufficiency. Objectives: To evaluate functional and morphological aspects of emphysematous rat lungs, prior to and following lung volume reduction surgery. Method: Wistar rats were divided into two experimental groups (papain without surgery and papain with surgery) and three control groups (saline without surgery, saline with surgery and papain without mechanical ventilation). After approximately 40 days of endotracheal instillation of papain or saline solution, animals in the papain with surgery and saline with surgery groups were submitted to bilobectomy of the middle lobes by right thoracotomy along the posterior border of the superior vena cava. After 1 week, the same animals were submitted to a mechanical ventilation study, which involved measurement of lung elasticity and airway resistance. For all of the animals studied, lung tissue was analyzed in order to determine alveolar diameter and the elastic fiber quantity. Results: Morphometric analysis revealed higher mean alveolar diameter in the lungs of all animals exposed to papain as compared to those exposed to saline. Elastic fiber counts in the alveolar septa of animals treated with papain were lower than those of animals receiving saline. In the animals submitted to bilobectomy and papain, lung elasticity was greater than in those receiving papain without surgery and was statistically equal to that seen in animals receiving saline (with or without surgery). Conclusion: In the respiratory systems of animals with pulmonary emphysema submitted to lung volume reduction by bilobectomy, the capacity for elastic recoil returned to values equivalent to those of the control group animals.

Keywords: Key words: Pulmonary emphysema. Papain/drugs efects. Case-control studies. Disease models, animal. Respiratory mechanics/drugs efects. Lung/sugery. Lung/anatomy & histology.

Introduction: Surgical procedures requiring aortic occlusion have been associated with pulmonary reperfusion injury. The authors studied the pulmonary edema in a reperfusion injury model by aortic occlusion in rats. Material and methods: Thirty-three Wistar rats were anesthetized with intraperitoneal injection of sodium pentobarbital (20 mg/kg). Using a midline abdominal incision, the infra-renal aorta was isolated and the animals were randomized into three groups. Ischemia-reperfusion group (IRG, n = 5): rats that underwent 30 min of aorta occlusion and were followed during 120 min of reperfusion. Ischemia group (IG, n = 5): rats that underwent 30 min of aorta occlusion. Control group (CG, n = 5): rats that underwent sham operations without aorta occlusion and were followed during 150 min. Histopathologic examination of the right lung was performed. The pulmonary edema was studied by morphometric analysis and so was the leukocytes infiltration. Eighteen rats (6 rats in each group) were studied with respect to lung fresh/dry weight ratio. ANOVA was used to analyze the morphometric results and the lung fresh/dry weight ratio, with Bonferroni adjustment for paired multiple comparisons. Animals of the IRG presented more pulmonary edema than those of the IG and CG (0.24 vs. 0.17 and 0.17, p < 0.001). There was no difference between the groups regarding the lung fresh/dry weight ratio. There were more inflammatory cells in the lungs of the rats submitted to ischemia-reperfusion. The authors concluded that infra-renal abdominal aorta cross-clamping and unclamping are associated with pulmonary edema. This edema is not induced by elevation of the hydrostatic pressure due to the aortic occlusion, since it was not seen in animals that were only submitted to ischemia.

Keywords: ischemia, reperfusion, pulmonary edema, inbred strains rats

Objective: To establish the incidence of acute lung injury and acute respiratory distress syndrome, as well as related risk factors and mortality in an intensive care unit. To compare patients developing lung injury with at-risk patients not presenting acute lung injury or acute respiratory distress syndrome. Methods: The study was conducted in the intensive care unit of the Ribeirão Preto Hospital das Clínicas Emergency Room. All patients admitted between May 2001 and April 2002 were monitored prospectively. Clinical data, Acute Physiologic and Chronic Health Evaluation II score, complications, length of stay in the intensive care unit and lung injury data were recorded. Results: Of the 524 patients admitted, 175 (33.4%) presented risk factors for acute lung injury and acute respiratory distress syndrome, 33 (6.3%) developed acute respiratory distress syndrome, and 12 (2.3%) developed acute lung injury. The main risk factors were pneumonia (37.7%), shock (32.0%), multiple trauma (24.6%) and sepsis (21.1%). Patients developing acute lung injury had higher Acute Physiologic and Chronic Health Evaluation II scores (p < 0.05), more frequently presented sepsis (p = 0.001), developed more complications (p = 0.001) and presented greater mortality (p = 0.001). The main cause of death was multiple organ failure (38.5%). Conclusion: The incidence of acute lung injury and acute respiratory distress syndrome was 2.3% and 6.3%, respectively.

Keywords: Respiratory distress syndrome, adult/epidemiology; Respiratory distress syndrome, adult/mortality;

Post-intubation tracheal injury is a rare and potentially fatal complication. Among the most common causes, cuff overinflation and repetitive attempts of orotracheal intubation in emergency situations are paramount. Diagnosis is based on clinical and radiological suspicion, confirmed by fiberoptic bronchoscopy. Both conservative and surgical management apply, and the decision-making process depends on the patient profile (comorbidities, respiratory stability), characteristics of the lesion (size and location) and the time elapsed between the occurrence of the injury and the diagnosis. We report the cases of three patients presenting tracheal laceration due to traumatic orotracheal intubation, two submitted to surgical treatment and one submitted to conservative treatment.

Keywords: Tracheal diseases; Rupture; Intubation.

The ischemia-reperfusion injury is a common pathophysiologic phenomenon in many diseases seen in daily clinical practice. The lung can be affected both directly, as in pulmonary edema after lung transplant or after resolution of pulmonary thromboembolism, and indirectly, as in shock states or after reperfusion injury in distant organs as intestine or lower extremities. The latter situation can occur secondary to aortic occlusion for surgical procedures. Many mediators have been implicated in the ischemia-reperfusion injury: oxygen free radicals, lipid products as thromboxane, adhesion molecules involved in leukocyte-endothelial interaction, tumor necrosis factor, among others. Therapeutic strategies for the reperfusion injury are used only at the experimental level and in very few clinical studies. Antioxidants, inhibitors of lipid mediators and of the leukocyte-endothelial interaction and promoters of blood flow in post-ischemic vessels have been used.

Keywords: Lung. Injury. Reperfusion. Ischemia.