Effects of hot electron emission on a low-conductivity tetracyanoethylene polymer layer including studies of the corrugation of the film surface.

The effect of strong field electron emission (FEE) on a tetracyanoethylene (TCNE) polymer layer was studied by Field Ion Microscopy (FIM) using TCNE and Ne as the imaging gases. The TCNE polymer was formed on each tungsten tip by radical polymerisation before FEE. The FIM images show field emission spots all over the surface of the tip. The FEM images show a random distribution of several field emission areas at the onset of FEE. After sometime at a current of about microA, there is a transition to higher currents at the same voltage, in which the electron emission pattern changes to have only one emitting area. After this transition, two different types of FIM images were observed, depending on the imaging gas that was used. Neon FIM images at low tip voltages show spots in the areas where the electron emission current was greatest, and at much higher voltages these images show emission from other areas with lower surface corrugation. However, the FIM images with TCNE as the imaging gas do not show any differences between the areas with and without electron emission. The FIM images remain as before FEE, which can be explained by the formation of a new polymer by the reaction of the surface layer with the imaging gas. It is assumed that chemically reactive fragments at the polymer/vacuum interface, which are needed for the polymerisation reaction, are formed by pyrolysis and sputtering processes during FEE.

Sublethal endotoxemia promotes pulmonary cytokine-induced neutrophil chemoattractant expression and neutrophil recruitment but not overt lung injury in neonatal rats.

Gram-negative sepsis and septic shock remain major causes of morbidity and mortality in the newborn. Respiratory failure is a common feature in neonatal sepsis regardless of the presence or absence of associated pneumonia. In adult animal models, cytokine-induced neutrophil chemoattractant (CINC) is a potent chemoattractant for neutrophils and believed to play a role in endotoxin-induced lung injury. We examined this in a neonatal model. Ten-day-old Sprague-Dawley rats were injected with Salmonella enteritidis endotoxin (ETX) 0.03 mg/kg i.p. and sacrificed at baseline, 30 min, 1, 2, 4, 8 and 16 h post-ETX. Blood was collected by cardiac puncture. After bronchoalveolar lavage, lung tissue was collected and evaluated for neutrophil (polymorphonuclear leukocyte) recruitment by myeloperoxidase assay (MPO). Lung CINC expression was measured by Northern blot and ELISA. Peripheral blood leukocytosis was noted at 1 h (p < 0.001) with counts below baseline at 2 and 4 h. Differential counts revealed neutrophilia at 8 h (p < 0.001). MPO revealed pulmonary PMN recruitment peaking at 1 h (p < 0.05) and CINC RNA and protein expression peaked slightly later at 2 h (p < 0. 001). No overt lung injury was noted by bronchoalveolar lavage cell counts or by histology. Therefore, pulmonary CINC expression and neutrophil recruitment follows LPS exposure in neonatal rats. This may represent priming of the lung tissue and a secondary event may be necessary for injury to occur.

Potentiation of the effects of sodium nitroprusside and of isoproterenol by selective phosphodiesterase inhibitors.

This study identified a series of alkylated xanthines and a papaverine analogue with a range of potencies and selectivities as inhibitors of phosphodiesterases isolated from bovine coronary arteries. The abilities of these inhibitors to potentiate the relaxant effects of sodium nitroprusside (SNP) and isoproterenol were predictable from the potencies to inhibit the calmodulin-sensitive and the cyclic AMP-specific forms of phosphodiesterase, respectively. Although the xanthines potentiated the SNP- and isoproterenol-induced increases in cyclic GMP and cyclic AMP, respectively, in manners that were consistent with the involvement of the respective cyclic nucleotides in the relaxation process, the papaverine analogue did not potentiate isoproterenol-induced increases in cyclic AMP levels. These data are consistent with the hypothesis that increases in cyclic GMP levels are responsible for the relaxation of coronary artery strips by SNP. In addition, the data indicate that the calmodulin-sensitive phosphodiesterase activity does not contribute significantly to the hydrolysis of cyclic AMP in the intact bovine coronary artery smooth muscle cells.