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缺氧及缺氧适应对家兔肺表面活性物质代谢的影响

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高原医学杂志 1989年第2期 19-24页

作者：程海军事医学科学院卫生学环境医学研究所

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肺疾患与分泌代谢紊乱

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天津医药 1987年第1期 123-125页

作者：刘又宁中国人民解放军总医院

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Conditional expression of fibroblast growth factor-7 in the developing and mature lung

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第16期275卷 11858-11864页

作者： Tichelaar, JW Lu, W Whitsett, JK Childrens Hosp Med Ctr Div Pulm Biol Cincinnati OH 45229 USA

Effects of fibroblast growth factor-7 (FGF-7) on lung morphogenesis, respiratory epithelial cell differentiation, and proliferation mere assessed in transgenic mice in which the human FGF-7 cDNA was controlled by a conditional promoter under the direction of regulatory elements from either the human surfactant protein-C (SP-C) or rat Clara cell secretory protein (ccsp) genes. Expression of FGF-7 was induced in respiratory epithelial cells of the fetal lung by administration of doxycycline to the dam. Prenatally, doxycycline induced FGF-7 mRNA in respiratory epithelial cells in both Sp-c and Ccsp transgenic lines, increasing lung size and causing cystadenomatoid malformation. Postnatally, mice bearing both Ccsp-rtta and (Teto)(7)-cmv-fgf-7 transgenes survived, and lung morphology was normal, Induction of FGF-7 expression by doxycycline in the Ccsp-rtta x (Teto)(7)-cmv-fgf-7 mice caused marked epithelial cell proliferation, adenomatous hyperplasia, and pulmonary infiltration with mononuclear cells. Epithelial cell hyperplasia caused by FGF-7 was largely resolved after removal of doxycycline. Surfactant proteins, TTF-1, and aquaporin 5 expression were conditionally induced by doxycycline. The Sp-c-rtta and Ccsp-rtta activator mice provide models in which expression is conditionally controlled in respiratory epithelial cells in the developing and mature lung, altering lung morphogenesis, differentiation, and proliferation.

关键词：水通道蛋白质5 水孔蛋白质类/代谢多西环素/药理学酶抑制剂/代谢上皮细胞/代谢成纤维细胞生长因子10 成纤维细胞生长因子7 成纤维细胞生长因子基因表达调控发育期生长物质/生物合成生长物质/遗传学原位杂交肺/生长和发育膜蛋白质类小鼠转基因核蛋白质类/代谢磷脂酶A/拮抗剂和抑制剂蛋白质类/遗传学蛋白质类/代谢蛋白脂质类/遗传学蛋白脂质类/代谢肺表面活性剂/遗传学肺表面活性剂/代谢转录因子/代谢转基因子宫珠蛋白/代谢动物人类小鼠大鼠

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Inhibition of lung surfactant protein B expression during Pneumocystis carinii pneumonia in mice

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JOURNAL OF LABORATORY AND CLINICAL MEDICINE 1999年第5期133卷 423-433页

作者： Beers, MF Atochina, EN Preston, AM Beck, JM Univ Penn Sch Med Dept Med Div Pulm & Crit Care Philadelphia PA 19104 USA Univ Michigan Sch Med Dept Internal Med Div Pulm & Crit Care Med Ann Arbor MI USA Vet Affairs Med Ctr Ann Arbor MI USA

The pathogenesis of Pneumocystis carinii pneumonia (PCP) suggests an important role for dysfunction of the pulmonary surfactant system in the hypoxemic respiratory insufficiency associated with this infection. Surfactant protein B (SP-B) is a hydrophobic protein shown to be essential for normal surfactant function in vivo. Therefore, we hypothesized that the inhibition of SP-B expression occurs during PCR and we tested this hypothesis in two immunodeficient animal models. PCP was induced in C,B-17 scid/scid mice by intratracheal inoculation of P carinii organisms. Infected lung homogenates, obtained at time points up to 6 weeks after inoculation, were analyzed for SP-B and mRNA content. When a comparison was made with uninfected scid controls, the densitometric quantitation of Western blots of lung homogenates demonstrated significant reductions in 8 kd SP-B in mice infected with P carinii 4 weeks after inoculation (16% of the control value). Northern blot analysis showed a concomitant decrease in SP-B mRNA to 24% of the control level. The decrease in SP-B and mRNA levels in lung homogenates of infected mice was reflected in lower SP-B levels in the surfactant, An enzyme-linked immunosorbent assay for the SP-B level in surfactant prepared from bronchoalveolar lavage samples of infected scid mice demonstrated a significant reduction in alveolar SP-B content (45% of the control value). In contrast to the results with SP-B, neither the SP-A protein content nor the mRNA level was significantly altered by PCP infection. To confirm these observations, SP-B expression was studied in an additional animal model of PCP. The SP-B content of lung homogenates from BALB/c mice depleted of CD4+ T cells and infected with Fl carinii was also reduced (51% of the control value). We conclude that P. carinii induces selective inhibition of the expression of SP-B in two mouse models of PCP and that this down-regulation is mediated at the level of mRNA expression. Therefore, an acquired d

关键词：支气管肺泡灌洗液/化学 CD4阳性T淋巴细胞/免疫学疾病模型动物减量调节基因表达调控肺/代谢小鼠近交BALBC 小鼠 SCID 肺炎肺囊虫性/病因学肺炎肺囊虫性/免疫学肺炎肺囊虫性/代谢蛋白脂质类/分析蛋白脂质类/遗传学蛋白脂质类/代谢肺表面活性物质相关蛋白质A 肺表面活性物质相关蛋白质类肺表面活性剂/分析肺表面活性剂/遗传学肺表面活性剂/代谢 RNA 信使/分析呼吸功能不全/病因学动物人类小鼠

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Inhaled nitric oxide decreases hyperoxia-induced surfactant abnormality preterm rabbits

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PEDIATRIC RESEARCH 1999年第2期45卷 247-254页

作者： Issa, A Lappalainen, U Kleinman, M Bry, K Hallman, M Univ Oulu Dept Pediat FIN-90220 Oulu Finland Univ Calif Irvine Dept Pediat Div Neonatal Med Irvine CA 92717 USA Univ Calif Irvine Dept Community & Environm Med Irvine CA 92717 USA Vanderbilt Univ Dept Pediat Div Neonatal Med Nashville TN USA

Inhaled nitric oxide (iNO) is a specific pulmonary vasodilator. By serving as a pro-oxidant or antioxidant, iNO may influence other pulmonary functions as well. This study was designed to test the hypothesis that iNO affects the alveolar lining after premature birth. Preterm rabbits (gestation 29 d, term 31 d) were nose-only exposed NO (14 ppm) and 98% O-2 for 20 h. The others were exposed to either 98% O-2 or air. In another experiment, premature rabbits were exposed to either NO in air or to air. After the exposure, bronchoalveolar lavage (BAL) was per formed and the surfactant aggregates were isolated. The surfactant components and surface activity were analyzed. In total, 144 animals were studied. There were no significant differences in the number, distribution, or respiratory burst activity of cells recovered by BAL. Neither brief hyperoxia nor iNO increased plasma-derived proteins in BAL. Exposure to O-2 decreased large surfactant aggregates, surface activity, and the content of surfactant protein B in BAL, whereas iNO prevented completely or partially these effects of acute hyperoxia on surfactant. Hyperoxia increased the content of malondialdehyde and decreased glutathione in epithelial lining fluid. iNO decreased malondialdehyde (p < 0.05) and tended to increase glutathione (p = 0.06) in animals breathing O-2. Nitrotyrosine was not detectable in BAL, and NO2 was low in the breathing area. In room air, iNO had no significant effect on surfactant. According to the present results, a brief period of hyperoxia causes an oxidant stress and decreases the surface activity of alveolar surfactant in premature rabbits. In contrast, a low dosage of iNO decreased or prevented the O-2-induced detrimental effects on alveolar surfactant and alleviated the oxidant stress.

关键词：投药吸入方差分析动物新生支气管肺泡灌洗支气管肺泡灌洗液/化学孕龄谷胱甘肽/代谢高氧症/病理生理学巨噬细胞肺泡/药物作用巨噬细胞肺泡/生理学一氧化氮/投药和剂量一氧化氮/药理学肺泡/药物作用肺泡/代谢肺表面活性剂/代谢参考值呼吸爆发动物兔

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Lung injury and surfactant metabolism after hyperventilation of premature lambs

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PEDIATRIC RESEARCH 2000年第3期47卷 398-404页

作者： Ikegami, M Kallapur, S Michna, J Jobe, AH Childrens Hosp Med Ctr Div Pulm Biol Cincinnati OH 45229 USA

We asked whether lung injury and surfactant metabolism differed in preterm lambs after a 1-h period of hyperventilation to PCO2 values of 25-30 mm Hg. The lambs then were surfactant treated and conventionally ventilated (CV) or high-frequency oscillatory ventilated (HFOV) for an additional 1 or 8 h. The results were compared with lambs that were not hyperventilated or surfactant treated but were ventilated with CV or HFOV. The 1-h hyperventilation resulted in increased alveolar protein, increased recovery of intravascular [I-131]albumin in the lungs, and an increase in tumor necrosis factor-alpha mRNA. Then were no differences between CV or HFOV in alveolar or total lung recoveries of saturated phosphatidylcholine (Sat PC), tracer doses of [C-14]Sat PC and [I-125]surfactant protein-B, or in percent Sat PC in large aggregate surfactant in surfactant-treated lambs. The lambs not hyperventilated or treated with surfactant had lower large aggregate pools and lower recoveries of [C-14]Sat PC and [C-14]surfactant protein-B in total lungs than for the surfactant-treated lungs, but there were no differences between the CV and HFOV groups. Hyperventilation followed by surfactant treatment resulted in a mild injury, but the subsequent use of CV or HFOV did not result in differences in surfactant metabolism.

关键词：肺/胚胎学肺/代谢肺损伤肺表面活性剂/代谢 RNA 信使/遗传学绵羊/胚胎学肿瘤坏死因子α/遗传学动物

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The lipids of pulmonary surfactant: Dynamics and interactions with proteins

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PROGRESS IN LIPID RESEARCH 1998年第4期37卷 235-276页

作者： Batenburg, JJ Haagsman, HP Univ Utrecht Vet Biochem Lab Grad Sch Anim Hlth NL-3508 TD Utrecht Netherlands Univ Utrecht Inst Biomembranes NL-3508 TD Utrecht Netherlands

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Alveolar proteinosis: a disease of mice and men

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AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 2001年第3期280卷 L377-L378页

作者： Carraway, MS Piantadosi, CA Wright, JR Duke Univ Med Ctr Dept Med Durham NC 27710 USA Duke Univ Med Ctr Dept Cell Biol Durham NC 27710 USA

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Pseudomonas aeruginosa from patients with cystic fibrosis affects function of pulmonary surfactant

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PEDIATRIC RESEARCH 2000年第1期47卷 121-126页

作者： Lema, G Dryja, D Vargas, I Enhorning, G SUNY Coll Buffalo Dept Obstet Gynecol Buffalo NY 14222 USA SUNY Coll Buffalo Dept Pediat Buffalo NY 14222 USA

Patients with cystic fibrosis are severely affected by an infection with Pseudomonas aeruginosa, a microbe known to synthesize phospholipase C. This study was designed to determine whether that enzyme would affect the function of pulmonary surfactant phospholipids. Mucoid and nonmucoid strains of P. aeruginosa, freshly obtained from patients with cystic fibrosis, were cultured for 12 h on agar plates. The bacteria were suspended in saline solution and then pelleted by centrifugation. The supernatant was used to dilute the surfactant preparation, calf lung surfactant extract, from 35 to 2 mg/mL. Surfactant function, before and after incubation, was examined with a capillary surfactometer, an instrument specifically developed for an evaluation of the ability of surfactant to maintain patency of a narrow glass tube, simulating a terminal conducting airway. Phospholipid hydrolysis was also evaluated biochemically by determining the total content of phospholipids in surfactant before and after incubation. In five experiments, the lipids were separated with thin-layer chromatography, and the phosphorus content was determined in the diacylphosphatidylcholine band before and after incubation for 6, 24, and 48 h. Capillary openness and phospholipid concentration decreased as enzyme concentration and time of incubation increased (p < 0.0001). Linear regression showed a significant correlation between time of capillary openness and phospholipid concentration (r = 0.957;p < 0.0001). Calf lung surfactant extract hydrolysis was catalyzed by extracts of the bacteria, particularly the nonmucoid, analogous to the catalysis observed with phospholipase C. Surfactant hydrolysis catalyzed by enzymes from P. aeruginosa might severely affect surfactant function provided enzyme concentration is high and time of incubation is long.

关键词：囊性纤维化/微生物学水解作用假单胞菌铜绿/分离和提纯假单胞菌铜绿/生理学肺表面活性剂/代谢肺表面活性剂/生理学人类

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Pulmonary surfactant proteins insert cation-permeable channels in planar bilayers

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MOLECULAR GENETICS AND METABOLISM 2000年第4期70卷 295-300页

作者： Oelberg, DG Xu, F Eastern Virginia Med Sch Ctr Pediat Res Norfolk VA 23510 USA Childrens Hosp Kings Daughters Ctr Pediat Res Norfolk VA 23510 USA Childrens Hosp Kings Daughters Dept Pediat Norfolk VA 23510 USA Univ Virginia Hlth Sci Ctr Dept Internal Med Div Cardiovasc Charlottesville VA 22903 USA

Pulmonary surfactant, a mixture of lipids and proteins, promotes lung ventilation by reduction of surface tension at air-fluid interfaces. Exogenous surfactants containing hydrophobic proteins induce biological effects in lungs that are not fully explained by reduction of surface tension and are not induced by surfactants lacking proteins. We hypothesized that hydrophobic proteins from surfactant insert in membranes to induce channel activities that contribute to the observed biological effects of surfactant. To test for channel insertion by surfactant, planar lipid bilayers were monitored electrophysiologically in the presence of either intact pulmonary surfactant or extracted surfactant proteins reconstituted with phospholipids or directly added to bilayer lipids prior to membrane casting. In this in vitro model, both intact surfactant and extracted surfactant proteins initiated gated channel activities with slope conductances averaging 40 pS. Observed reversal potentials confirmed monovalent cation conductance, and conductance of smaller monovalent cations was selective. Voltage dependence of channel openings and rectification of channel current were not observed. These results confirm that hydrophobic surfactant proteins induce channel-mediated transport in artificial membranes. We speculate that pulmonary surfactants, in addition to reducing surface tension at air-fluid interfaces, initiate physiological and therapeutic effects in lung by cation channel insertion at exposed epithelial membranes. (C) 2000 Academic Press.

关键词：阳离子离子通道/代谢脂双层肺表面活性剂/代谢

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