morphine and Lung-Neoplasms

Meconium aspiration syndrome (MAS) is a cause of significant morbidity and mortality in the perinatal period. Despite the clinical relevance of MAS, its pathogenesis is poorly understood. Epithelial cell-derived prostanoids are involved in the regulation of several cellular functions within the lung, including the control of tone and reactivity of airway and vascular smooth muscle. In this study, we evaluated whether exposure to meconium affects the metabolic function of human airway epithelial cells. Monolayers of A549 cells, a transformed human epithelial cell line, were incubated with various concentrations of meconium. Control cells were incubated with serum-free medium in a similar manner. The supernatant fluid was removed at various time points and assayed for thromboxane A(2) (TXA(2)) production. The latter was accomplished by measuring its immediate and stable metabolite thromboxane B(2), using an enzyme-linked immunosorbent assay (ELISA). In selected experiments, the modulatory effects of indomethacin (10(-6) M), dexamethasone (10(-6) M), and L-nitroarginine methyl ester (L-NAME, 10(-6) M) on TXA(2) production were evaluated. Results were expressed in terms of pg/mg protein (mean +/- SE). We found that exposure to meconium produced a significant release of TXA(2) from A549 cells. Indomethacin, dexamethasone, and in part, L-NAME inhibited meconium-induced release of TXA(2). Our findings demonstrate that meconium enhances the production of thromboxanes from A549 cells, suggesting that airway epithelial cells and their metabolic products may play an important role in the pathogenesis of MAS.

Topics: Dexamethasone; Epithelial Cells; Humans; Indomethacin; Infant, Newborn; Lung Neoplasms; Meconium; NG-Nitroarginine Methyl Ester; Thromboxane A2; Tumor Cells, Cultured

Human alpha fetoprotein (AFP) has been detected by the agar double diffusion method in ascitic fluid, cerebrospinal fluid (CSF) and bile, from fetuses, neonates and patients with AFP seropositive hepatocellular carcinoma. AFP was detected in the meconium and faeces of fetuses and neonates respectively. The protein was not detected in the amniotic fluid nor the pericardial fluid. It was found in the urine in only two fetuses that had concomittant renal disease. It was not detected in breast milk of lactating females. When metastases occurred in the lung from a hepatocellular carcinoma producing AFP, the pleural effusions sometimes contained AFP. The concentrations of AFP in the serum and in the other body fluids were about the same. This indicates that other body fluids can be used for the diagnosis of hepatocellular carcinoma.

Topics: Adult; Amniotic Fluid; Animals; Ascitic Fluid; Bile; Body Fluids; Carcinoma, Hepatocellular; Feces; Female; Fetal Proteins; Fetus; Humans; Immunodiffusion; Infant, Newborn; Liver Neoplasms; Lung Neoplasms; Meconium; Middle Aged; Milk, Human; Neoplasm Metastasis; Pericardial Effusion; Pleural Effusion; Rabbits