Effect of methylprednisolone on perivascular pulmonary edema, inflammatory infiltrate, VEGF and TGF-beta immunoexpression in the remaining lungs of rats after left pneumonectomy

Pneumonectomy is associated with high rates of morbimortality, with postpneumonectomy pulmonary edema being one of the leading causes. An intrinsic inflammatory process following the operation has been considered in its physiopathology. The use of corticosteroids is related to prevention of this edema, but no experimental data are available to support this hypothesis. We evaluated the effect of methylprednisolone on the remaining lungs of rats submitted to left pneumonectomy concerning edema and inflammatory markers. Forty male Wistar rats weighing 300 g underwent left pneumonectomy and were randomized to receive corticosteroids or not. Methylprednisolone at a dose of 10 mg/kg was given before the surgery. After recovery, the animals were sacrificed at 48 and 72 h, when the pO2/FiO2 ratio was determined. Right lung perivascular edema was measured by the index between perivascular and vascular area and neutrophil density by manual count. Tissue expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-β) were evaluated by immunohistochemistry light microscopy. There was perivascular edema formation after 72 h in both groups (P = 0.0031). No difference was observed between operated animals that received corticosteroids and those that did not concerning the pO2/FiO2 ratio, neutrophil density or TGF-β expression. The tissue expression of VEGF was elevated in the animals that received methylprednisolone both 48 and 72 h after surgery (P = 0.0243). Methylprednisolone was unable to enhance gas exchange and avoid an inflammatory infiltrate and TGF-β expression also showed that the inflammatory process was not correlated with pulmonary edema formation. However, the overexpression of VEGF in this group showed that methylprednisolone is related to this elevation

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO2/FiO2 ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity.Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)CNP

The Incidence Of Residual Pneumothorax After Video-assisted Sympathectomy With And Without Pleural Drainage And Its Effect On Postoperative Pain [incidência De Pneumotórax Residual Após Simpatectomia Torácica Videotoracoscópica Com E Sem Drenagem Pleural E Sua Possível Influência Na Dor Pós-operatória]

Objective: To determine the incidence of residual pneumothorax after video-assisted thoracic sympathectomy, with and without postoperative pleural drainage, and to evaluate the possible influence of this type of pneumothorax on postoperative pain within the first 28 postoperative days. Methods: All patients presenting symptoms consistent with primary palmoplantar hyperhidrosis and treated at the Thoracic Surgery Outpatient Clinic of the State Hospital of Sumaré between July and December of 2006 were included. All were submitted to sympathectomy up to the third ganglion using video-assisted thoracoscopy and were randomized to receive or not receive postoperative pleural drainage for 3 h. Chest X-rays and low-dose computed tomography scans of the chest were performed on the first postoperative day in order to determine the incidence of residual pneumothorax. At different time points up to postoperative day 28, patient pain was assessed using a visual numeric scale and by measuring the quantity of opioid analgesics required. Results: This study comprised 56 patients, 27 submitted to bilateral pleural drainage and 29 not submitted to drainage. There was no statistical difference between the two groups in terms of the incidence of post-sympathectomy residual pneumothorax. Residual pneumothorax diagnosed through any of the methods did not influence pain within the first 28 postoperative days. Conclusion: Performing closed pleural drainage for 3 h immediately after video-assisted thoracic sympathectomy did not affect lung re-expansion or the incidence of residual pneumothorax. 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