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内毒素诱导的山羊红细胞膜和肝线粒体膜Ca2+-ATP酶活性的改变及654-2的保护作用 总被引：1，自引：0，他引：1
通过静脉注射的方法研究了大肠杆菌内毒素(ET)对山羊红细胞膜和肝粒体膜损伤的膜Ca2+-ATP酶活性的变化及654-2(山莨菪碱)的保护效应。结果表明,ET处理组(ⅱ组)在1h,3h红细胞膜Ca2+-ATP酶活性高于对照组(iv组)(p<0.05),5h有下降趋势且持续到9h.12h开始回升并低于iv组(p<0.01,p<0.05).654-2处理组(ⅲ组),Ca2+-ATP酶活性除在9h、12h与iv组,在3h与ⅱ组差异不显着(p>0.05)外,均高于iv组和ⅱ组(p<0.01,p<0.05).在肝线粒体中,ⅱ组Ca2+-ATP酶活性在5h、12h均低于iv组和ⅱ组(p<0.05,p<0.01),ⅲ组Ca2+-ATP酶活性均高于iv组,但12h与iv组差异不显着(p>0.05).结果提示,ET具有诱导膜Ca2+-ATP酶活性先激活后顿抑的效应,而654-2有明显保护膜Ca2+-ATP酶活性的作用。 相似文献
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本文通过给山羊静注大肠杆菌内毒素诱导内毒素休克,探讨内毒素休克时血液流变性的变化规律,并观察山莨菪碱（６５４－２）对其影响。结果表明,山羊内毒素休克时,低切率全血比粘度（ＬＢＶ）和低切率全血还原比粘度（ＬＢＲＶ）明显升高（Ｐ＜０．０５）,血浆比粘度（ＰＶ）和红细胞聚集指数（ＡＩ）均显著增高（Ｐ＜０．０１,Ｐ＜０．０５）,红细胞变形能力（ＲＣＤ）显著下降（Ｐ＜０．０５,Ｐ＜０．０１）,当静注内毒素前１０ｍｉｎ给予６５４－２（２．５ｍｇ／ｋｇ）山羊的ＬＢＶ和ＬＢＲＶ在１～５ｈ显著高于对照组,５ｈ前ＰＶ和ＡＩ值比对照组有明显升高,第７ｈ后与对照组间无明显差异（Ｐ＞０．０５）,且显著低于休克组（Ｐ＜０．０５）,其ＲＣＤ亦趋于正常。提示山羊内毒素休克时血液流变参数明显改变,血液粘度增加,红细胞聚集加剧,而应用６５４－２具有显著改变血液状态,缓解微循环障碍发生。 相似文献
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内毒素对山羊红细胞膜ATPase活性的影响及654—2的保护效应 总被引：5，自引：0，他引：5
通过静脉注射的方法研究了大肠杆菌仙毒素对山羊红细胞膜损伤的膜泵分子活性的变化及６５４－２（山莨菪碱）的保护效应。结果表明,ＥＴ处理组在１ｈ,３ｈ红细胞膜Ｎａ＾＋－Ｋ＾＋ＡＴＰａｓｅ（腺苷三磷酸酶,简称ＡＴＰ酶）,Ｃａ＾２＋,Ｍｇ＾２＋－ＡＴＰａｓｅ活性均高于对照组,５ｈ有下降趋势并一直持续到９ｈ。 相似文献
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通过静脉注射的方法研究了大肠杆菌内毒素（ＥＴ）对山羊红细胞膜和肝粒体膜损伤的膜Ｃａ２＋－ＡＴＰ酶活性的变化及６５４－２（山莨菪碱）的保护效应．结果表明,ＥＴ处理组（Ⅱ组）在１ｈ,３ｈ红细胞膜Ｃａ２＋－ＡＴＰ酶活性高于对照组（Ⅰ组）（ｐ＜００５）,５ｈ有下降趋势且持续到９ｈ．１２ｈ开始回升并低于Ⅰ组（ｐ＜００１,ｐ＜００５）．６５４－２处理组（Ⅲ组）,Ｃａ２＋－ＡＴＰ酶活性除在９ｈ、１２ｈ与Ⅰ组,在３ｈ与Ⅱ组差异不显著（ｐ＞００５）外,均高于Ⅰ组和Ⅱ组（ｐ＜００１,ｐ＜００５）．在肝线粒体中,Ⅱ组Ｃａ２＋－ＡＴＰ酶活性在５ｈ、１２ｈ均低于Ⅰ组和Ⅱ组（ｐ＜００５,ｐ＜００１）,Ⅲ组Ｃａ２＋－ＡＴＰ酶活性均高于Ⅰ组,但１２ｈ与Ⅰ组差异不显著（ｐ＞００５）．结果提示,ＥＴ具有诱导膜Ｃａ２＋－ＡＴＰ酶活性先激活后顿抑的效应,而６５４－２有明显保护膜Ｃａ２＋－ＡＴＰ酶活性的作用． 相似文献
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AIM: To observe the changes of interleukin-6(IL-6), IL-8 and tumor necrosis factor-α(TNF-α) in serum and lung at different time, and the effects of anisodamine (654-2) treatment in rats with oleic acid-induced ARDS. METHODS: The ARDS model induced by intravenous injection of oleic acid in the rat was used and levels of IL-6, IL-8, TNF-α in serum and lung tissue supernatant were measured using enzyme linked immunosorbent assay (ELISA). RESULTS: Levels of serum and lung tissue IL-6, IL-8, TNF-α in oleic acid type ARDS 4 h group were increased significantly. These cytokines in oleic acid type ARDS 8 h group were lower than that of ARDS 4 h group, but serum IL-6, TNF-α and lung tissue IL-6 were still higher than that of control group . In oleic acid type ARDS 16 h group, serum IL-6, TNF-α were lower than that of the ARDS 8 h group and serum TNF-α and lung tissue IL-6 were higher than that of control group. After 654-2 treatment, the levels of serum and lung tissue IL-6, TNF-α were decreased significantly. CONCLUSION: IL-6, IL-8 and TNF- α might play important roles in the oleic acid-induced ARDS in the rat. 654-2 might alleviate ARDS by inhibiting excess production of IL-6 and TNF-α. 相似文献
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AIM: To study the effects of cyproheptadine (Cyp) and anisodamine (Ani) on the changes of intracellular free Ca2+ concentration ([Ca2+]i) induced by tumor necrosis factor (TNFα) in single endothelial cells, and to explore the mechanisms of TNFα mediated shock and antishock actions of Cyp and Ani. METHODS: Human umbilical vein endothelial cell strains (ECV304) were seed in 35 mm tissue culture dish with 2 mL DMEM culture medium. The cultured cells were loaded by Fluo-3/AM. The spatial distribution and the dynamic changes of [Ca2+]i in single endothelial cell was determined by laser scanning confocal microscopy (LSCM). RESULTS: [Ca2+]i in single endothelial cell after stimulation of TNFα rapidly increased in a dose-dependent manner and approached the peak value within 60 seconds, afterwards, decreased and kept above the basal level. The confocal scanning image showed that [Ca2+]i elevation was more obvious in nuclear than in cytoplasma, and decreased slowly. Cyp (3×10-5, 6×10-5 mol/L) and Ani (2×10-5, 4×10-5 mol·L-1) markedly inhibited TNFα (1.2×10-9 mol·L-1)-induced [Ca2+]i elevation. CONCLUSIONS: TNFα markedly induces elevation of [Ca2+]i in single endothelial cell, it may be an important mechanism of TNFα-induced shock and tissue injury. Cyp and Ani obviously suppress TNFα-induced [Ca2+]i elevation, which probably is one of the mechanisms of their antishock effects. 相似文献
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