Coal is of heterogeneous nature with a complex chemical structure, which is closely associated with its reactivity. In this research, from the perspective of the chemical structure of coal, reaction characteristics of the as-synthesized CuFe 2 O 4 oxygen carrier (OC) with a typical Chinese bituminous coal (designated as LZ) were deeply investigated using thermogravimetric analysis (TGA). Also, the effect of CuFe 2 O 4 oxygen excess number Φ on the reaction behavior of LZ coal with CuFe 2 O 4 was highlighted. TGA investigation of LZ coal reaction with CuFe 2 O 4 at Φ = 1.0 displayed the enhanced reactivity of CuFe 2 O 4 , which was useful to conversion of the aromatic matrix in LZ coal. Furthermore, during LZ coal reaction with CuFe 2 O 4 in the TGA, the gaseous products evolved from the condensed flue gas were in situ analyzed using Fourier transform infrared (FTIR), which indicated that most of the CO 2 resulted from oxidation of CO by CuFe 2 O 4 OC. Meanwhile, the solid product left after LZ coal reaction with CuFe 2 O 4 was analyzed with X-ray photoelectron spectroscopy (XPS), which revealed that oxidation and conversion of the C−C/C−H groups was the limited step at the molecular scale for full conversion of coal. Finally, the effect of CuFe 2 O 4 excess number Φ for LZ coal reaction with CuFe 2 O 4 was investigated by TGA, and the solid product left was analyzed by XPS, which indicated that C−C/C−H was more effectively converted at CuFe 2 O 4 Φ = 1.0 than Φ = 0.5 and 1.5 at the final reaction temperature of 900 °C. In addition, the mechanism of coal oxidation by CuFe 2 O 4 was also explored, and the C−C/C−H involved in LZ coal was preferentially oxidized to form C−O groups and then further converted to OC−O groups through the formed intermediate CO groups. Overall, this research was much beneficial for a mechanistic understanding of the conversion of coal in a CLC system and promotion of the efficient utilization of coal.
This study was designed to examine the in vivo and in vitro effects of captopril, an angiotensin-converting enzyme inhibitor, on nicotine-induced endothelial dysfunction in rats. Endothelial dysfunction was induced by exposing isolated rat mesenteric arteries to nicotine (0.01, 0.1, or 1 mM) for 24 hr using an organ culture system, or by treating rats with nicotine (2 mg/kg/day, intraperitoneally) for 4 weeks. The protective effects of captopril were tested by exposing isolated mesenteric arteries to captopril (0.01, 0.03, or 0.1 mM) π nicotine (0.1 mM) for 24 hr, or by treating rats with captopril (3 mg/kg/day, intravenously) π nicotine (2 mg/kg/day, intraperitoneally) for 4 weeks. Exposure of the isolated mesenteric arteries to nicotine induced a significant concentration -dependent inhibition of endothelium-dependent relaxation. Co-culture of segments of mesenteric artery with captopril (0.03 or 0.1 mM) attenuated the nicotine-induced impairment of vasorelaxation in a dose-dependent manner. Administration of nicotine to rats for 4 weeks significantly impaired endothelium-dependent relaxation compared with control rats. This impairment was accompanied by a reduction in nitrite/nitrate, nitric oxide (NO) synthase (NOS), and superoxide dismutase (SOD) activities in the serum and aorta. Chronic captopril treatment not only improved the impairment of endothelium-dependent relaxation, but also prevented the reduction of nitrite/nitrate contents and of NOS and SOD activities in the serum and aorta. However, there were no significant differences in serum angiotensin-converting enzyme activity among the three groups. These results indicate that captopril can be used to attenuate nicotine-induced endothelial dysfunction, an effect that may be related not only to antioxidation, but also to enhancing NO production by preventing the decrease in NOS.
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