氰戊菊酯气管注入染毒后大鼠支气管肺泡灌洗液中LDH活性…

本文通过检测大鼠支气管肺泡灌洗液中ＬＤＨ总活性及ＬＤＨ同功酶改变，从时间和剂量两个方面对吸入氰戊菊酯的毒性作用作了探讨。结果表明：染毒后１天支气管肺泡灌洗液中ＬＤＨ４，ＬＤＨ５含量均升高，第１４天恢复正常，酶谱改变较ＬＤＨ总活性变化敏感。     

大容量肺灌洗对家兔肺脏影响的研究

模拟临床大容量肺灌洗方法，用生理盐水对家兔进行右肺灌洗。结果显示：灌洗后３天支气管肺泡灌洗液中总磷脂、二棕榈酰卵磷脂含量明显降低，蛋白质含量增高；灌洗后即刻的肺形态学表现为肺泡结构轻度紊乱等；１５天时，上述变化均趋于恢复。提示：大容量肺灌洗可因所致肺表面活性物质大量丢失及肺组织形态学改变而对肺脏产生一定影响。     

矽肺大鼠支气管肺泡灌洗的排出物动态变化及其在治疗中的意义

支气管肺泡灌洗术(BAL)已应用于临床治疗尘肺,但进展不快,主要是对其可行性和可能性仍有异议。为促进BAL这一新方法在矽肺治疗中的应用,本实验通过对不同柒尘时间矽肺大鼠支气管肺泡灌洗液(BALF)中排出物含量动态变化观察,就其可能性进行探讨。实验结果表明:不同染尘时间实验组BALF中的细胞总数、LDH活性、总蛋白含量均高于对照组,且有非常显著差别(P<0.01),尤以来尘7、15、30天差异更为显著。提示:BAL可以洗出大量细胞及非细胞成份,对减轻肺泡炎、减少肺部损伤将有积极作用,且以早期或急性矽肺施行BAL为宜。     

染尘大鼠肺灌洗液与血清及肺生化变化间关系

本文研究不同粉尘对大鼠支气管肺泡灌洗液、血清及肺脏的某些影响及相互关系。选用健康成年雄性Wistar大鼠,分新康温石棉,石棉矿精选车间自然积尘、石英、钛尘和正常对照组、每组6只,经一次性非暴露式气管染尘,各组每只动物注入相应粉尘悬液50mg/ml,对照组注入生理盐水1 ml。三个月后股动脉放血处死,分离出血清,测定铜兰蛋白(CP)及羟脯氨酸(HOP)、乳酸脱氢酶(LDH)、和酸性磷酸酶(ACP)。并按无菌操作、常规解剖,用定量生理盐水灌洗获取支气管肺泡灌洗液,分离出肺泡巨噬细胞(AM),并作培养计数,灌洗液和培养液进一步测定LDH和ACP。然后将全肺经105℃烘干,测肺重、总脂及胶原。结果上述所测各项指标数值经方差分析,各实验组间均有非常显著差异,且均以石英组最高,积尘组和石棉组次之,对照照最低。同时对上述各组肺组织、血清及灌洗液三部分材料的多项指标的测定值作相关分析,表明灌洗液中AM、LDH与ACP的数值与肺胶原、肺总脂、CP、HOP均有非常显著相关。而且从灌洗液、细胞培养液及血清中分别测得的LDH相互又有显著相关。故认为,以灌洗液尤其AM与LDH测定,了解尘肺受损情况是较好的指标和具有实用价值,值得进一步研究推广。     

双光气吸入染毒后大鼠肺泡Ⅱ型细胞变化的动态观察

本实验动态观察了双光气吸入染毒后大鼠肺泡Ⅱ型细胞的变化，分析了支气管肺泡灌洗液（ＢＡＬＦ）中碱性磷酸酶（ＡＫＰ）活性和总磷脂（ＴＰ）含量。结果表明，吸入双光气后大鼠ＢＡＬＦ中ＡＫＰ活性和ＴＰ含量的改变与肺泡Ⅱ型细胞的变化密切相关，并提示鼠肺对双光气所致肺损伤有很强的修复能力。     

矽宁对实验性矽肺磷脂变化的影响

应用高效液相色谱分析法，对实验性矽肺大鼠的支气管肺泡灌洗液、肺泡巨噬细胞及肺组织的磷脂组分进行动态观察，并探讨抗矽肺新药矽宁对磷脂作用的特点。实验结果表明：实验性矽肺支气管肺泡灌洗液中的总蛋白及总磷脂含量伴随矽肺纤维化病变的进展而出现逐步增长的趋势。在这些生物样品的磷脂组分中，以ＰＣ含量增长最为明显，其次为ＰＥ及ＳＰＨ。矽宁治疗组的支气管肺泡灌洗液中磷脂含量明显低于矽肺对照组，且其ＰＥ／ＳＰＨ及ＰＣ／ＳＰＨ组分的比值高于矽肺对照组，但肺泡巨噬细胞中的这种比值都低于矽肺对照组。本实验提示矽宁的疗效作用可能与抑制磷脂合成、改变其各组分含量有一定关系。     

双光气吸入染毒后大鼠肺泡Ⅱ细胞变化的动态观察

本实验动态观察了双光气吸入染毒后大鼠肺泡Ⅱ型细胞的变化，分析了支气管肺泡灌洗液（ＢＡＬＦ）中碱性磷酸酶（ＡＫＰ）活性和总磷脂（ＴＰ）含量。结果表明，吸入双光气后大鼠ＢＡＬＦ中ＡＫＰ活性和ＴＰ含量的改变与肺泡Ⅱ型型细胞的变化密切相关，并提示鼠肺对双光气所致肺损伤有很强的修复能力。     

支气管肺泡灌洗术排出肺内滞留物治疗矽肺大鼠的实验研究

支气管肺泡灌洗术(BAL)已用于临床尘肺治疗,但其进展不快,原因之一是由于 BAL 能否用于尘肺治疗仍有争议。为促进 BAL 在尘肺治疗中应用.本实验观察不同染尘时间矽肺大鼠(?)气管肺泡灌洗液(BALF)中排出物的动态变化,并对 BAL 作用机制进行初步探讨。实验结果表明:不同染尘时间的矽肺大鼠BALF 中细胞总数、LDH 活性,总蛋白和 LPO 含量均高于对照组.且差别有非常显著意义。染尘后早期,7、15、30天上述指标与染尘后180天相比,差别也有显著或非常显著意义,提示:不同染尘时期的矽肺大鼠经 BAL 均可洗出一定量炎症细咆、蛋白质和 LPO。可见,BAL 通过其机械清洗作用,使蓄积在肺泡腔内的有害物质排出体外。对减轻和缓解矽肺病变的发生发展将有积极的作用。     

环境卫生与监测

981768吸烟对人支气管肺泡灌洗液及肺泡巨噬细胞血管紧张素I转换酶活性的影响/陈 乎…//中华结核和呼吸杂志.一1997,20(2).一l】9～120 对12例健康非吸烟者和15例健康吸烟者进行了支气管肺泡灌洗液(BALF)中及肺泡巨噬细胞(AM)的血管紧张素I转换酶(ACE)活性变化研究:结果:与健康     

大鼠肺部对正-己烷和X线单独或联合作用的反应

作者进行实验研究,将大鼠分为三组。第1组单独吸入正-己烷5500mg/m~3,每天5小时,共计8天;第2组单独照射4GyX线;第3组吸入正-己烷后立即照射X线,然后对三个组大鼠进行生化、细胞学和形态学检查。 结果见短时间吸入正-已烷会在支气管肺泡的灌洗液中增加总细胞数,尤其是肺泡巨噬细胞更为增加。LDH及碱性磷酸酶活性的增加在最初阶段显     

2,4,5-T effects on cardiac and serum lactic dehydrogenase (LDH) and creatine kinase (CK) isozymes II. Neonatal enzyme activities and isozyme profiles

Neonates from CD-1 mice, which were treated during gestation with 100 mg/kg of 2,4,5-T, were studied from day 1 to 30 postpartum (pp) for effects on cardiac development by determining total cardiac activities and isozyme profiles of LDH and CK. On day 1pp, the total activities and isozyme profiles of LDH of the neonatal hearts were normal. During the developmental period of day 7 through 15, changes were noted in the developmental pattern of LDH isozymes some of which continued to day 30. The CK isozyme profile on day 1pp showed a significant change and changes continued throughout the lactational period. During this period, the normal developmental isozyme patterns of LDH and CK were altered by prenatal exposure to 2,4,5-T suggesting metabolic derangement or pathological changes in the neonatal heart.     

Effects of Asian dust event particles on inflammation markers in peripheral blood and bronchoalveolar lavage in pulmonary hypertensive rats

The health impact of dust events from China has become a concern within China and in its neighboring countries. Previous epidemiological studies have demonstrated an association between particulate matter exposure and cardiopulmonary mortality. Here, we use pulmonary hypertensive rat models to examine inflammation markers in the lung and in peripheral blood after exposure to Asian dust storm particles. Using a nose-only inhalation system, eight pulmonary hypertensive rats were exposed to concentrated ambient particles (CAPs) from an actual Asian dust storm that took place between March 18 and 19, 2002; four control rats were also exposed to room air. Four rats exposed to CAPs of 315.6 g/m3 for 6 h were classified as the low-exposure group, and another four rats exposed to CAPs of 684.5 g/m3 for 4.5 h were classified as the high-exposure group. The animals were sacrificed 36 h after exposure. Inflammation markers in the peripheral blood and in the bronchoalveolar lavage (BAL) were analyzed, and IL-6 in BAL was also determined using ELISA. White blood cell counts in peripheral blood increased with increased CAP exposure levels (P<0.001, test for trend). In BAL analysis, total cell numbers and the proportion of neutrophil also increased with increased CAP levels (P<0.001, test for trend for both markers). Positive dose-response relationships between CAP exposure and total protein (P<0.05) and between CAPs and LDH activity (P<0.05) were also observed. Moreover, IL-6 protein in BAL increasing with CAP levels (P<0.05, test for trend) was demonstrated. Our results revealed that exposure to particulate matters during an Asian dust storm could increase lung inflammation and injury in pulmonary hypertensive rats. Further studies are needed to determine the components of dust storm particles that may contribute to the particle toxicity.     

Inhaled concentrated ambient particles are associated with hematologic and bronchoalveolar lavage changes in canines

Pulmonary inflammatory and hematologic responses of canines were studied after exposure to concentrated ambient particles (CAPs) using the Harvard ambient particle concentrator (HAPC). For pulmonary inflammatory studies, normal dogs were exposed in pairs to either CAPs or filtered air (paired studies) for 6 hr/day on 3 consecutive days. For hematologic studies, dogs were exposed for 6 hr/day for 3 consecutive days with one receiving CAPs while the other was simultaneously exposed to filtered air; crossover of exposure took place the following week (crossover studies). Physicochemical characterization of CAPs exposure samples included measurements of particle mass, size distribution, and composition. No statistical differences in biologic responses were found when all CAPs and all sham exposures were compared. However, the variability in biologic response was considerably higher with CAPs exposure. Subsequent exploratory graphical analyses and mixed linear regression analyses suggested associations between CAPs constituents and biologic responses. Factor analysis was applied to the compositional data from paired and crossover experiments to determine elements consistently associated with each other in CAPs samples. In paired experiments, four factors were identified; in crossover studies, a total of six factors were observed. Bronchoalveolar lavage (BAL) and hematologic data were regressed on the factor scores. Increased BAL neutrophil percentage, total peripheral white blood cell (WBC) counts, circulating neutrophils, and circulating lymphocytes were associated with increases in the aluminum/silicon factor. Increased circulating neutrophils and increased BAL macrophages were associated with the vanadium/nickel factor. Increased BAL neutrophils were associated with the bromine/lead factor when only the compositional data from the third day of CAPs exposure were used. Significant decreases in red blood cell counts and hemoglobin levels were correlated with the sulfur factor. BAL or hematologic parameters were not associated with increases in total CAPs mass concentration. These data suggest that CAPs inhalation is associated with subtle alterations in pulmonary and systemic cell profiles, and specific components of CAPs may be responsible for these biologic responses.     

Tumor necrosis factor-alpha release from rat pulmonary leukocytes exposed to ultrafine cobalt:in vivo andin vitro studies

Ultrafine cobalt (Uf-Co), one of the new category of ultrafine particles, is generated in some industrial situations and it also exists in environmental particles. The aim of this study was to investigate the ability of rat pulmonary leukocytes to release tumor necrosis factor alpha (TNF-alpha) after exposure to Uf-Coin vivo andin vitro. Rats were intratracheally instilled with 1 mg of Uf-Co, and then wet lung weight and bronchoalveolar lavage fluid (BALF) profile were analysed 1, 3, 7, 15, and 30 days later. The effects of Uf-Co on indices that can be presumed to reflect epithelial injury and permeability (lactate dehydrogenase (LDH) and total protein (TP)) were increased throughout the 30 day post-exposure period. Furthermore, at 3 days after exposure, leukocytes were collected by bronchoalveolar lavage (BAL). After 3, 6, 12, 24, 48, and 72 hours of incubation, TNF-alpha in supernatants were determined by ELISA method. The results showed that TNF-alpha secretion by activated leukocytes from rats instilled with Uf-Co was significantly higher than that of the controls. BAL leukocytes from the lung of exposed rats revealed time-arid dose-related increases in TNF-alpha release. In conclusion, our results reveal, for the first time to our knowledge, that exposure to Uf-Co can stimulate leukocytes to secrete TNF-alpha. These data suggest that the TNF- alpha release from pulmonary leukocytes probably plays a role in the pathogenesis of “cobalt lung”.     

Cell response in bronchoalveolar lavage fluid after sulfur dioxide exposure

Environmental chamber exposure and bronchoalveolar lavage (BAL) were used to study the dose-response relationship between short-term exposure to sulfur dioxide (SO2) and inflammatory reactions in the human lung as reflected in BAL fluid. Healthy subjects were exposed to 10, 13, 20, or 30 mg/m3 for 20 min. BAL was performed several weeks preexposure and 24 h postexposure. Mast cells, lymphocytes, lysozyme positive macrophages, and the total number of macrophages were significantly increased after SO2 exposure. A dose-dependent increase in the cell response in BAL fluid was observed after exposure to 10-20 mg/m3, but no further increase was detected after 30 mg/m3. Inflammatory cell response was found in BAL fluid at SO2 levels that occur in industrial indoor environments worldwide, and cell response to SO2 was also seen below the short-term exposure limit of Sweden and many other countries (13 mg/m3).     

煤尘职业接触者和早期煤工尘肺BAL液中表面活性物质研究

目的 探讨煤尘职业接触者和早期煤工尘肺患者BAL液中表面活性物质含量改变特点及其意义。方法 采煤工人23人,按X线诊断煤工尘肺期别分为0期（煤尘接触者）组7人、0^ 组8人和I期组8人,并取健康农民7人为对照组。经纤维支气管肺泡灌洗（BAL）收集BAL液,测定表面活性蛋白A(SP－A）和磷脂（PL）及其组分含量。结果 0期组BAL液中SP－A含量、SP－A／PL和PG／PI明显高于对照组（P＜0．01）,且随煤工尘肺期别增加而有降低趋势。结论 BAL液中SP－A含量、SP－A／PL和PG／PI升高可能是煤尘接触的早期效应指标。     

Inhalation exposure study of titanium dioxide nanoparticles with a primary particle size of 2 to 5 nm

BACKGROUND: Nanotechnology offers great promise in many industrial applications. However, little is known about the health effects of manufactured nanoparticles, the building blocks of nanomaterials. OBJECTIVES: Titanium dioxide (TiO(2)) nanoparticles with a primary size of 2-5 nm have not been studied previously in inhalation exposure models and represent some of the smallest manufactured nanoparticles. The purpose of this study was to assess the toxicity of these nanoparticles using a murine model of lung inflammation and injury. MATERIALS AND METHODS: The properties of TiO(2) nanoparticles as well as the characteristics of aerosols of these particles were evaluated. Mice were exposed to TiO(2) nanoparticles in a whole-body exposure chamber acutely (4 hr) or subacutely (4 hr/day for 10 days). Toxicity in exposed mice was assessed by enumeration of total and differential cells, determination of total protein, lactate dehydrogenase (LDH) activity and inflammatory cytokines in bronchoalveolar lavage (BAL) fluid. Lungs were also evaluated for histopathologic changes RESULTS: Mice exposed acutely to 0.77 or 7.22 mg/m(3) nanoparticles demonstrated minimal lung toxicity or inflammation. Mice exposed subacutely (8.88 mg/m(3)) and necropsied immediately and at week 1 or 2 postexposure had higher counts of total cells and alveolar macrophages in the BAL fluid compared with sentinels. However, mice recovered by week 3 postexposure. Other indicators were negative. CONCLUSIONS: Mice subacutely exposed to 2-5 nm TiO(2) nanoparticles showed a significant but moderate inflammatory response among animals at week 0, 1, or 2 after exposure that resolved by week 3 postexposure.     

Reductions in lymphocyte subpopulations after repeated exposure to 1.5 ppm nitrogen dioxide.

In this investigation the effects of repeated exposure to 1.5 ppm NO2 on immune competent cells in bronchoalveolar lavage (BAL) fluid was studied. Special attention was focused on effects on lymphocyte subpopulations. Eight healthy subjects were exposed to 1.5 ppm NO2 every second day on six occasions. Bronchoalveolar lavage fluid was collected at least three weeks before the exposure series as reference and 24 hours after the last exposure. The results obtained were analysed using a non-parametric test for paired observations, with each subject as his own control. Significant reductions were found in the total number and percentage of T cytotoxic-suppressor cells in BAL fluid; this caused an increase in the ratio of T helper-inducer: cytotoxic-suppressor cells. The total number of natural killer cells in the BAL fluid was also reduced. The numbers of all other cell types were unchanged after exposure. No reduction of phagocytosis of opsonised yeast particles by alveolar macrophages in vitro was detected. It is concluded that repeated short term exposures to 1.5 ppm NO2, a moderate occupational concentration, induces significant effects on immune competent bronchoalveolar lymphocytes. This indicates that previous findings of changes in the lymphoid immune system induced by NO2 in animals may well be applicable to humans.     

Reductions in lymphocyte subpopulations after repeated exposure to 1.5 ppm nitrogen dioxide.

In this investigation the effects of repeated exposure to 1.5 ppm NO2 on immune competent cells in bronchoalveolar lavage (BAL) fluid was studied. Special attention was focused on effects on lymphocyte subpopulations. Eight healthy subjects were exposed to 1.5 ppm NO2 every second day on six occasions. Bronchoalveolar lavage fluid was collected at least three weeks before the exposure series as reference and 24 hours after the last exposure. The results obtained were analysed using a non-parametric test for paired observations, with each subject as his own control. Significant reductions were found in the total number and percentage of T cytotoxic-suppressor cells in BAL fluid; this caused an increase in the ratio of T helper-inducer: cytotoxic-suppressor cells. The total number of natural killer cells in the BAL fluid was also reduced. The numbers of all other cell types were unchanged after exposure. No reduction of phagocytosis of opsonised yeast particles by alveolar macrophages in vitro was detected. It is concluded that repeated short term exposures to 1.5 ppm NO2, a moderate occupational concentration, induces significant effects on immune competent bronchoalveolar lymphocytes. This indicates that previous findings of changes in the lymphoid immune system induced by NO2 in animals may well be applicable to humans.