谷氨酸钠对实验性矽肺大鼠肺冲洗液中脂质含量的影响

本文报告了谷氨酸钠对矽肺大鼠肺冲洗液中脂质含量的影响。实验分为正常对照、矽肺、预防性治疗及病后治疗组,疗程150天。实验结果表明,谷氨酸钠治疗组大鼠肺冲洗液中脂质含量明显低于矽肺组(P<0.05～0.01),并且治疗组大鼠肺冲洗液中脂质含量的变化与全肺胶原蛋白含量及病理变化相平行,均低于同期矽肺组。     

不同变质期煤尘致病作用的实验研究

在广西四个不同煤矿矿井下回采工作面采集新鲜无烟煤、烟煤及褐煤，制成煤尘后对Ｗｉｓｔａｒ大鼠进行非暴露式一次染尘。染尘４５天及９０天时宰杀大鼠进行实验研究。结果：大鼠肺冲洗液中脂质含量、鼠肺干、湿重及全肺胶原含量，石英组（阳性对照）大于煤尘组，煤尘组大于生理盐水组（阴性对照），差异有显著性意义（Ｐ＜０．０１）；煤尘组间的差异与其变质程度的高低无关。提示石英尘的致病性比煤尘强，煤尘致病性的强弱与其变质程度的高低无相关关系。     

不同变质期煤尘致病作用的实验研究

在广西四个不同煤矿矿井下回采工作面采集新鲜无烟煤、烟煤及褐煤,制成煤尘后对Wistar大鼠进行非暴露式一次染尘。染尘45天及90天宰杀大鼠进行实验研究。结果:大鼠肺冲洗液中脂质含量、鼠肺干、湿重及全肺胶原含量,石英组(阳性对照)大于煤尘组,煤尘组大于生理盐水组(阴性对照),差异有显著性意义(P<0.01);煤尘组间的差异与其变质程度的高低无关。提示石英尘的致病性比煤尘强,煤尘致病性的强弱与其变质程度的高低无相关关系。     

广西不同煤质和围岩粉尘对大鼠肺纤维化病变的研究

目的：探讨不同煤种煤尘致病性的特点，确定影响煤尘致病性的主要因素。方法：采用广西烟煤、无烟煤和褐煤不同煤种粉尘制作大鼠尘肺模型，从生化指标来探讨不同的煤种粉尘与尘肺的发病关系。结果：染尘大鼠肺冲洗液中酸性磷酸酶、乳酸脱氢酶，肺组织中脂质过氧化物、胶原蛋白含量均为石英组最高，其次依次是烟煤组、无烟煤组、褐煤组，最低为正常对照组，结果差异有显著性（P＜0．01）。结论：围岩煤尘具有一定的致病性，但较石英弱，其致病性强弱与煤质优劣无关，与围岩煤尘中游离二氧化矽的含量高低有一定关系。     

柠檬酸铝对矽肺大鼠肺冲洗液中脂质含量的影响

本文报告了柠檬酸铝对矽肺大鼠肺冲洗液中脂质含量的影响。实验分为正常对照、矽肺及柠铝治疗组,疗程180天。实验结果表明,柠铝治疗组大鼠肺冲洗液中脂质含量明显低于矽肺组。本文还对实验结果做了讨论阐述。     

4种粉尘对大鼠损伤作用的研究

采用非暴露式气管注入染毒的方式研究燃煤尘，冶金尘，建筑材料尘和自然尘对大鼠肺的损伤作用，结果表明，燃煤尘组大鼠肺泡巨噬细胞微核率明显增高，说明其具有一定的致突作用，燃煤尘，冶金尘，建筑尘均对大鼠肺组织产生一定的损伤作用，具体表现在染毒后大鼠肺灌洗液中乳酸脱氢酶，酸性磷酸酶活性和唾液酸含量的增高以及肺组织中脂质过氧含量的增高和谷胱甘肽过氧化物酶活性下降，但从作用强度来看，燃煤尘的毒作用不大冶金尘和建     

大鼠实验性矽肺后期肺冲洗液中脂质和肺胶原蛋白含量变化的观察

为了进一步探讨实验性矽肺后期的脂质、肺胶原蛋白等指标的变化规律,我们观察了大鼠染尘后期(180～270天)的肺冲洗液中脂质含量和肺胶原蛋白含量的变化,以对矽肺的发病过程提供一定的理论依据。     

吸入含矽粉尘和煤尘在大鼠肺中滞留的比较研究

以大鼠动式吸入染尘方法吸入含矽尘和煤尘２周。用甲酸消化法测定大鼠肺和纵膈淋巴结中的粉尘含量。结果发现在染尘结束后的第３天，煤尘组大鼠肺中的粉尘含量高于矽尘组；９０天后则矽尘组大鼠肺中的粉尘含量高于煤尘组。提示含矽粉尘在肺中滞留较煤尘持久，因而可对肺产生较为严重的损伤。结果也同时证实淋巴系统是肺内粉尘转移的一条重要途径。     

维生素E对大鼠矽肺支气管肺灌洗液中几种磷脂含量的影响

本文报告了维生素E对大鼠矽肺支气管肺泡灌洗液中几种磷脂含量的影响。实验分为正常对照,石英及维生素E治疗组,疗程270天。结果表明,维生素E组肺灌洗液中总磷脂、二棕榈酰卵磷脂(DPPC)、磷脂酰甘油三酯(PG)、磷脂酰乙醇胺(PE)含量早期高于同期对照组,但又都低于同期石英组。维生素E组全肺胶原蛋白含量高于对照组,但均低于同期石英组。提示维生素E在抗脂质过氧化、保护生物膜及抑制胶原合成上起着一定的作用。     

汉防己甲素对矽肺大鼠肺内脂类含量的影响

本文比较了正常大鼠、矽肺大鼠和汉防己甲素不同时间治疗的矽肺大鼠肺组织、肺冲洗物的湿重和脂类含量的差异。矽肺鼠肺组织、肺冲洗物的湿重和脂类含量均比正常鼠高,肺表面活性物增高显著;汉防己甲素治疗的矽肺大鼠肺组织、肺冲洗物湿重和脂类含量均较矽肺大鼠的低,肺表面活性物减低显著,但仍较正常鼠高。本文对其结果作了讨论,提出肺重肺脂可作为粉尘毒性指标,试图解释肺脂增高与肺纤维化的关系以及汉防己甲素的作用原理。     

Effect of silica on lipid peroxidation in the red cells

Summary The influence of five varieties of silica dust on lipid peroxidation in erythrocytes was studiedin vitro. Control tests were performed on samples of erythrocytes not exposed to dust, which were hemolyzed by freezing and thawing, and on corundum-treated red cells. The amounts of the lipid peroxides produced after 1 hr incubation were measured by means of the thiobarbituric-acid test (TBA). All the varieties of silica dust investigated induced a significantly higher level of lipid peroxides than was found in the control samples. The hemolysis produced by silica dusts was associated with the formation of an appreciable amount of malonaldehyde, indicating peroxidative cleavage of the polyunsaturated fatty acids. Pretreatment of the dusts with polyvinylpyridine-N-oxide (PVPNO) prevented any enhancement of lipid peroxidase activity. The results obtained suggest that lipid peroxidation of membrane-bound polyunsaturated fatty acids may be involved in the cytotoxic activity of SiO₂ dust. The damaging effect of silica dust on cells is discussed in the light of the theory of electron catalysis and in terms of damage to membranes by free radicals.     

Development of silicotic lesions in the lungs of rats pre-exposed to coal fly ash

The development of silicotic lesions was studied in the lungs of rats pre-exposed to a pulmonary load of coal fly ash. Exposure to quartz alone increased the wet weight, dry weight, and collagen content of the lungs. These changes were associated with an increase in the activity of lactate dehydrogenase, total proteins, and the cellularity of bronchoalveolar lavage. When the lungs of rats were pre-exposed to coal fly ash for 60 days and then exposed to quartz dust for periods similar to those used for exposure to quartz alone, the development of silicotic lesions and the laying down of collagen fibres was retarded, as judged by histopathological examination and biochemical analysis of the tissues for hydroxyproline contents. These changes in the lung tissue were associated with a significant reduction in the level of lactate dehydrogenase enzyme activity, total cell counts, and protein contents of the bronchoalveolar lavage derived from rats exposed to quartz.     

Development of silicotic lesions in the lungs of rats pre-exposed to coal fly ash.

The development of silicotic lesions was studied in the lungs of rats pre-exposed to a pulmonary load of coal fly ash. Exposure to quartz alone increased the wet weight, dry weight, and collagen content of the lungs. These changes were associated with an increase in the activity of lactate dehydrogenase, total proteins, and the cellularity of bronchoalveolar lavage. When the lungs of rats were pre-exposed to coal fly ash for 60 days and then exposed to quartz dust for periods similar to those used for exposure to quartz alone, the development of silicotic lesions and the laying down of collagen fibres was retarded, as judged by histopathological examination and biochemical analysis of the tissues for hydroxyproline contents. These changes in the lung tissue were associated with a significant reduction in the level of lactate dehydrogenase enzyme activity, total cell counts, and protein contents of the bronchoalveolar lavage derived from rats exposed to quartz.     

N-acetylcysteine and deferoxamine reduce pulmonary oxidative stress and inflammation in rats after coal dust exposure

Coal dust inhalation induces oxidative damage and inflammatory infiltration on lung parenchyma. Thus, the aim of this study was to determine whether N-acetylcysteine (NAC) administered alone or in combination with deferoxamine (DFX), significantly reduced the inflammatory infiltration and oxidative damage in the lungs of rats exposed to coal dust. Forty-two male Wistar rats (200-250 g) were exposed to the coal dust (3mg/0.5 mL saline, 3 days/week, for 3 weeks) by intratracheal instillation. The animals were randomly divided into three groups: saline 0.9% (n=8), supplemented with NAC (20mg/kg of body weight/day, intraperitoneal injection (i.p.)) (n=8), and supplemented with NAC (20 mg/kg of body weight/day, i.p.) plus DFX (20 mg/kg of body weight/week) (n=8). Control animals received only saline solution (0.5 mL). Lactate dehydrogenase activity and total cell number were determined in the bronchoalveolar lavage fluid. We determined lipid peroxidation and oxidative protein damage parameters and catalase and superoxide dismutase activities in the lungs of animals. Intratracheal instillation of coal dust in the lungs of rats led to an inflammatory response and induced significant oxidative damage. The administration of NAC alone or in association with DFX reduced the inflammatory response and the oxidative stress parameters in rats exposed to coal dust.     

吸入对苯二甲酸粉尘大鼠肺表面活性物质的改变

用高效液相色谱法检测了动式吸入对苯二甲酸粉尘后大鼠支气管肺泡灌洗液中肺表面活性物质磷脂的含量,各实验组染尘几何平均浓度分别为８．９３,２７４．４５和６１８．１２ｍｇ／ｍ＾３。结果显示中,高剂量实验组磷脂酰胆碱,磷脂酰甘油,磷脂酰肌醇均较对照组减少,提示吸入对苯二甲酸粉尘可影响肺泡Ⅱ型上皮细胞肺表面活性物质的合成与分泌功能。     

A further experimental study of the antisilicotic effect of glutamate.

Two groups of rats were exposed to quartz dust for six months and in addition one group was given drinking water containing 1.5% sodium glutamate while the second received only water. In the rats receiving glutamate we observed (a) evidence for a considerably reduced cytotoxic effect of the quartz on cells obtained by bronchopulmonary lavage, (b) a reduction in dust retention in the lungs, especially in the tracheobronchial lymph nodes, (c) a considerable reduction in the weight gain in the lungs and in their hydroxyproline and lipid contents, and (d) the inhibition of the formation of silicotic nodules. Polarographic studies of the oxygen consumption of peritoneal macrophages from rats receiving glutamate showed that glutamate prevents the adverse effects of quartz on mitochondrial oxidative processes.     

Effect of NO2 inhalation and vitamin C deficiency on protein and lipid accumulation in the lung

Vitamin C-deficient and normal guinea pigs were exposed to various concentrations of NO₂ or air, and lavage fluid was obtained and analyzed for protein and lipid content. Exposure of normal animals to 752, 1880, 5640, or 9400 μg NO₂/m³ (0.4, 1.0, 3.0, or 5.0 ppm) for 72 hr did not alter the protein or lipid content of lung lavage fluid. However, exposure of vitamin C-deficient animals to the same concentrations of NO₂ caused marked increases in lavage proteins and lipids at all but the 752 μg/m³ (0.4 ppm) level. At 9400 μg NO₂/m³ (5.0 ppm), 50% of the exposed vitamin C-deficient animals died, and pathologic study of the lungs showed proteinaceous edema fluid in the alveoli. Lungs from air-exposed animals and normal animals exposed to NO₂ appeared healthy. No effects were seen at 752 μg NO₂ (0.4 ppm) in either normal or deficient animals even when the time of exposure was extended to 1 week. At 9400 μg NO₂/m³ (5 ppm) effects could be seen in vitamin C-deficient animals even when the exposure period was shortened to 3 hr. Assessment of protein and lipid content of lavage fluid provided a sensitive method for determining subtle changes in the lung following NO₂ exposure.