RESUMO
BACKGROUND: Acute pulmonary thromboembolism is fatal because of abruptly occurring hypoxemia and right ventricular failure. There are several treatment modalities, including anticoagulation, thrombolytics, ECMO (extracorporeal membrane oxygenator), and thromboembolectomy, for managing acute pulmonary thromboembolism. MATERIALS AND METHODS: Medical records from January 1999 to December 2004 at our institution were retrospectively reviewed for pulmonary thromboembolectomy. There were 7 patients (4 men and 3 women), who underwent a total of 8 operations because one patient had post-operative recurrent emboli and underwent reoperation. Surgery was indicatedfor mild hypoxemia and performed with CPB (cardiopulmonary bypass) in a beating heart state. RESULTS: The patients had several symptoms, such as dyspnea, chest discomfort, and palpitation. Four patients had deep vein thromboembolisms and 3 had psychotic problems, specifically schizophrenia. Post-operative complications included hemothorax, pleural effusion, and pericardial effusion. There were two hospital deaths, one each by brain death and right heart failure. CONCLUSION: Emergency operation should be performed when medical treatments are no longer effective.
RESUMO
To investigate whether amiodarone induces apoptosis in cells of the L-132 human lung epithelial cell line, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, 4,6-diamidino-2-phenylindole staining, DNA fragmentation assay, reverse transcription-polymerase chain reaction, and casapse-3 enzyme assay were performed. Through morphological and biochemical analyses, it was demonstrated that L-132 cells treated with amiodarone exhibit several features of apoptosis. In addition, it was shown that amiodarone increases the mRNA levels of bax and caspase-3. Based on the results, amiodarone appears to activate specific intracellular death-related pathways, including possibly the bax-dependent caspase-3 activation pathway, and thus induce apoptosis in human lung epithelial cells.
