实验性吸烟对胎鼠及幼鼠血清IGF-I的影响

目的用被动吸烟法建立宫内被动吸烟胎鼠及宫内至断乳前持续被动吸烟幼鼠动物模型,比较不同浓度香烟暴露对胎鼠及幼鼠血清IGF-I的影响。方法SD雌鼠于交配后第2d,入低、中、高三种香烟浓度的被动吸烟箱中,每日5h,孕21d剖宫取胎,收集胎鼠血清;或待孕鼠自然分娩,幼鼠置于与宫内相同香烟浓度的被动吸烟箱中,每日5h,至21d断乳,取幼鼠血清。结果不同浓度香烟暴露对胎鼠血清IGF-I的影响无显著差异,随香烟浓度增高幼鼠血清IGF-I呈下降趋势,高浓度组与对照组间差异显著。结论宫内至断乳前持续被动吸烟降低幼鼠血清IGF-I水平,随香烟浓度增高,差异显著。     

实验性吸烟对胎鼠及幼鼠血清IGF-Ⅰ的影响

目的用被动吸烟法建立宫内被动吸烟胎鼠及宫内至断乳前持续被动吸烟幼鼠动物模型 ,比较不同浓度香烟暴露对胎鼠及幼鼠血清IGF -Ⅰ的影响。　方法SD雌鼠于交配后第 2d ,入低、中、高三种香烟浓度的被动吸烟箱中 ,每日 5h ,孕 2 1d剖宫取胎 ,收集胎鼠血清 ;或待孕鼠自然分娩 ,幼鼠置于与宫内相同香烟浓度的被动吸烟箱中 ,每日 5h ,至 2 1d断乳 ,取幼鼠血清。　结果不同浓度香烟暴露对胎鼠血清IGF -Ⅰ的影响无显著差异 ,随香烟浓度增高幼鼠血清IGF -Ⅰ呈下降趋势 ,高浓度组与对照组间差异显著。　结论宫内至断乳前持续被动吸烟降低幼鼠血清IGF -Ⅰ水平 ,随香烟浓度增高 ,差异显著。     

实验性吸烟对胎鼠及幼鼠血清IGF—I的影响

目的 用被动吸烟法建立宫内被动吸烟胎鼠及宫内至断乳前持续被动吸烟幼鼠动物模型,比较不同浓度香烟暴露对胎鼠及幼鼠血清IGF－I的影响。方法 SD雌鼠于交配后第2d,入低、中、高三种香烟浓度的被动吸烟和箱中,每日5h,孕21d剖宫取胎,收集胎鼠血清;或待孕鼠自然分娩,幼鼠置于与宫内相同香烟浓度的被动吸烟箱中,每日5h,孕21d断乳,取幼鼠血清。结果 不同浓度香烟暴露对胎鼠血清IGF－I的影响无显著差异,随香烟浓度增高幼鼠血清IGF－I呈下降趋势,高浓度组对照间差异显著。结论 宫内至断乳前持续被动吸烟降低幼鼠血清IGF－I水平,随香烟浓度增高,差异显著。     

被动吸烟对幼鼠学习记忆的影响及党参液的保护作用

目的：探讨被动吸烟对幼鼠学习能力的影响及党参的拮抗作用。方法：跳台法和迷宫趋食法。结果：幼鼠长期吸入香烟烟雾后，条件反射的建立延迟，迷津学习成绩和跳台成绩都受到损害，潜伏期缩短，出错率增加，党参可以减弱上述损害。结论：长期吸入香烟烟雾会损害小鼠学习记忆能力，党参具有一定的保护作用。     

七氟烷对幼鼠脑细胞凋亡和远期学习记忆功能的影响

目的：观察幼鼠暴露于不同浓度七氟烷不同时间后,脑细胞凋亡及远期学习记忆、空间探索能力的变化,探讨脑细胞凋亡与认知功能障碍的关系。方法：出生后7 d的Wistar幼鼠21只随机分为7组行预实验,选出无二氧化碳蓄积的麻醉方案。出生后7 d的Wistar幼鼠90只随机分为5组：模拟麻醉（A组）、1%（体积分数）七氟烷麻醉2 h（B组）和4 h（C组）、2%（体积分数）七氟烷麻醉2 h（D组）和4 h（E组）,麻醉结束6 h后,每组6只幼鼠,多聚甲醛灌注取脑,免疫组织化学方法检测半胱氨酸天冬氨酸蛋白酶3（caspase-3）表达。其余幼鼠分别在成长至5、8、14周时,进行Morris水迷宫实验和避暗实验。结果：与A组相比,B、D及E组在海马齿状回及CA3区等脑区caspase-3阳性细胞数明显增加（P<0.05）。各组幼鼠各阶段Morris水迷宫观察指标差异无统计学意义（P>0.05）,七氟烷麻醉组在5周时避暗反应差于模拟麻醉组,第8周时与模拟麻醉组无差别。结论：发育期幼鼠暴露于2%七氟烷可诱发海马神经元凋亡,同时一过性影响幼鼠对不良刺激的记忆能力;暴露于2%七氟烷不会造成幼鼠空间记忆能力下降。     

孕鼠被动吸烟对仔鼠学习记忆的影响

目的　了解生命早期被动吸烟对学习记忆的影响。方法　两组实验动物分别在胚胎期和生后一个月内接触香烟烟雾,固定烟流量为２ Ｌ／ｍｉｎ 每日２ ｈ。３２ 日龄时,采用反映学习记忆能力的跳台试验测试小鼠幼鼠神经行为的改变。　结果宫内和生后一个月吸烟小鼠从放入电网到跳上跳台的时间分别明显较各自对照组长,而电网通电２ ｍｉｎ,吸烟小鼠在跳台上停留时间则分别显著地较各自对照组短。实验组仔鼠和幼鼠体重也明显低于对照组。结论　在生命早期被动吸烟对小鼠体质和智力发育有明显影响。     

热休克蛋白对惊厥性脑损伤保护作用的实验研究

目的：探索热休克蛋白对惊厥性脑损伤的保护作用及其可能机理。方法：采用美解眠腹腔注射在成年和幼年Wistar鼠中制成全身性惊厥模型，采用HE及TUNEL染色研究脑组织中神经元坏死及凋亡发生情况，并通过免疫组化技术检测惊厥发作后7d后不同时相点上，海马神经元内热休克蛋白70（HSP70）表达的动态规律；同时采用荧光分光光度法测定海马组织中一氧化氮浓度的变化。结果：长程惊厥发作后（1）未成年鼠脑内神经元死亡，尤其是神经元凋亡显著低于成年鼠；（2）成年鼠与幼鼠脑内的HSP70表达存在差异。成年鼠阳性率为65％，大多（77．5％）属低度阳性，24h即回到惊厥前水平；幼鼠HSP70表达阳性率为85％，且其中一半（52．5％）呈强阳性而持续至惊厥后72h。（3）幼鼠脑内NO浓度在发作后2h达峰值，24h后一直低于该对照组。结论：长程惊厥发作后，脑内HSP70的合成明显增加可能是未成熟脑对惊厥性脑损伤具有耐受性的一种重要神经生物学基础，可能通过抑制神经元凋亡及神经元内NO的合成而对神经元起到保护作用。     

被动吸烟致IUGR幼鼠小脑皮质NGF基因表达的改变

目的　了解宫内发育迟缓 (IUGR)幼鼠脑发育过程中神经生长因子 (NGF)在不同阶段的变化 ,探索IUGR时脑损伤的发生机制。方法　采用孕鼠被动吸烟的方法建立IUGR幼鼠动物模型 ,用免疫组化染色检测IUGR幼鼠出生时及生后第 8天时小脑皮质NGF的变化。结果　①IUGR幼鼠出生体重较正常对照组脑重降低 16 1%± 0 3 2 % (3 49g± 0 2 4g ,P <0 0 0 0 1) ;②IUGR幼鼠出生时脑重较正常对照组脑重降低 (0 15 6g± 0 0 12 g ,P <0 0 5 ) ;③IUGR幼鼠生后第 8天体重与正常对照组无差异 (P >0 0 5 ) ,但脑重与对照组有差异 (0 487g± 0 0 40 g ,P <0 0 5 ) ;④IUGR幼鼠出生时小脑皮质NGF蛋白较正常对照组降低 (P <0 0 0 5 ) ,且在生后第 8天仍有差异 (P <0 0 5 ) ,与脑重改变一致。结论　IUGR幼鼠脑发育落后的发生可能与脑NGF基因表达下降有关 ,并且NGF的降低持续时间长 ,在 8d以上。同时发现 ,IUGR幼鼠体格发育存在追赶性生长 ,而脑发育迟缓不易恢复     

被动吸烟大鼠生精细胞凋亡与Bcl-2、Bax表达的相关性研究

目的探讨被动吸烟对大鼠生精细胞凋亡和Bcl-2（B淋巴细胞瘤/白血病-2基因）、Bax（Bcl-2相关X蛋白）表达水平的影响,以及生精细胞凋亡与Bcl-2、Bax表达之间的相关性。方法用60日龄SD雄性大鼠40只建立被动吸烟大鼠模型,按染毒剂量不同随机均分为4组：0 g/m3组、6.49 g/m^3组、12.98 g/m^3组、25.96 g/m^3组,染毒剂量分别为0、1、2、4枝香烟,均每日2次,每次30 min,4周后处死。TUNEL检测凋亡,免疫组化（S-P法）检测Bcl-2、Bax表达。结果染毒组凋亡细胞数量增多。Bcl-2阳性表达随染毒剂量的增加呈下降趋势,Bax在染毒组中的表达明显要高于对照组,凋亡指数（AI）与Bax的表达强度呈正相关,与Bcl-2表达强度呈负相关。结论吸烟可致大鼠生精细胞凋亡,可能是通过Bcl-2表达下降、Bax表达升高,引发生精细胞凋亡增多。     

被动吸烟对怀孕小鼠胚胎发育的影响

目的　探讨被动吸烟对怀孕小鼠胚胎发育的影响及量效关系。方法　采用不同吸烟强度 (分别为每日5、10、2 0支 )处理怀孕期小鼠。怀孕 19天解剖孕鼠 ,观察胚胎数目、性别比例、胎重、胎盘重、畸形、死胎及吸收胎等。结果　随着吸烟量的增加 ,被动吸烟孕鼠胚胎总数无明显变化 (P >0 .0 5 ) ,吸收胎的百分率有增加趋势。胚胎重量和胎盘重量低于对照组 (P <0 .0 5 ) ,性别比例与对照组相比无显著差别 (P >0 .0 5 ) ,各组中均未发现畸胎。结论　在本实验条件下 ,怀孕期被动吸烟能够阻碍胚胎发育。     

吸烟慢性阻塞性肺疾病大鼠肺组织内质网相关凋亡基因Caspase-12的表达

目的观察吸烟COPD模型大鼠肺组织内质网相关凋亡基因半胱氨酸天冬氨酸蛋白酶12（Caspase-12）的基因和蛋白表达。方法 40只成年雄性Wistar大鼠随机分为对照组、吸烟2个月组、吸烟4个月组及戒烟1个月组。采用单纯被动吸烟法复制大鼠COPD模型。检测各组大鼠第0.3秒用力呼气容积与用力肺活量比值（FEV0.3/FVC）和呼气峰流速（PEF）。逆转录-聚合酶链反应（RT-PCR）检测肺内Caspase-12 mRNA表达,免疫组化、Western blot检测其蛋白表达,荧光酶标法检测其活性。结果大鼠吸烟2个月后,肺功能较对照组明显下降（P〈0.05）,肺结构出现破坏;吸烟4个月后,FEV0.3/FVC显著下降（P〈0.05）,肺结构破坏明显;戒烟1个月组肺功能较吸烟4个月组稍好转,肺结构破坏仍明显（P〉0.05）。与对照组比较,Caspase-12表达及活性在吸烟2个月大鼠模型中升高（P〈0.05）,在吸烟4个月大鼠中明显升高（P〈0.05）,在戒烟1个月组较吸烟4个月组稍下降但无显著差异（P〉0.05）。结论吸烟能够诱导肺内内质网相关凋亡基因Caspase-12表达增加,促进COPD的发生与发展。     

被动吸烟对大鼠心肌组织 心室结构及血清标志物的影响

目的 探讨被动吸烟对大鼠心肌组织、心室结构及血清标志物的影响。方法 将20只雄性SD大鼠随机分为两组：实验组予以被动吸烟,每周被动吸烟5d,2次/d,每次燃烧香烟10支;对照组予以正常空气对照。于4、8、12周时大鼠分别称重观察生长情况,并于8、12周时行心脏彩超,12周将大鼠处死,取血清检测脑钠肽及肌钙蛋白T的含量;心室行HE染色,观察大鼠心肌变化。结果 ①心室结构比较,实验组大鼠在12周时具有更大经体重调整后的左室舒张末期容积、收缩末期容积及室间隔厚度（P＜0.05）。②随着实验时间的延长,被动吸烟组大鼠的左室舒张末期容积增加（P＜0.05）。③实验组大鼠血清脑钠肽及肌钙蛋白T浓度明显增加（P＜0.001）。④大鼠心肌HE染色,实验组大鼠出现心室肌细胞纤维分离、淋巴细胞浸润及血管充血。结论 长期被动吸烟会导致大鼠心肌组织、心室结构改变及影响血清标志物浓度,进而影响心室重塑。     

高温与香烟联合对大鼠胚胎的毒性和致畸作用

目的探讨高温与香烟联合的胚胎毒性和致畸作用。方法用高温（40℃、41℃、42℃、43℃）、香烟烟雾水溶物及其联合处理孕10d的大鼠,孕20d后按致畸实验方法观察其胚胎的死亡率、吸收率和畸胎率。结果持续3min的高温（42℃）与香烟联合,胚胎致畸率达70％以上,与单独高温组、单独给烟组有明显差异（P＜0．01）。结论高温与香烟联合可加强胚胎的致畸作用,并与温度、香烟浓度和高温持续时间明显相关,持续高温与香烟联合有明显的胚胎毒性和致畸作用。     

Passive cigarette smoking and patients with asthma

A study of the effect of passive smoking on patients with asthma is presented. Six patients were exposed for one hour to the air in a room in which tobacco smoke was produced mechanically over that period. The effects on symptoms, lung function and airways sensitivity to inhaled histamine were then measured and compared with the same patient's responses during a control day when they inhaled smoke-free air. All six patients developed chest tightness and symptoms similar to an attack of asthma. The findings of respiratory and sensitivity tests suggest: (i) that passive smoking may trigger asthma attacks in subjects who suffer from asthma and (ii) that the airways of such subjects show increased histamine reactivity four hours after the passive smoke exposure.     

Cigarette smoking and exposure to passive smoke are risk factors for cervical cancer

Personal cigarette smoking and exposure to passive smoke as risk factors for cervical cancer were examined in a population-based, case-control study conducted in Utah. Personal cigarette smoking was found to increase the risk of cervical cancer, after adjusting for age, educational level, church attendance, and sexual activity. The adjusted risk estimate associated with being a current smoker was 3.42 (95% confidence interval [Cl], 2.10 to 5.57); for having smoked for 5 or more pack-years, it was 2.81 (95% Cl, 1.73 to 4.55); and for having smoked at least 100 lifetime cigarettes, it was 2.21 (95% Cl, 1.44 to 3.39). The adjusted risk estimate (also adjusted for actual cigarettes smoked) associated with passive smoke exposure for 3 or more hours per day was 2.96 (95% Cl, 1.25 to 7.03). Risk from passive smoking was greater in women who were not smokers (odds ratio, 3.43; 95% Cl, 1.23 to 9.54) than in women who smoked (odds ratio, 2.59; 95% Cl, 0.23 to 29.24).     

被动吸烟对大鼠肝脏功能影响的初步观察

目的 :观察被动吸烟对大鼠肝功能的影响。方法 :健康Wistar大鼠 16只 ,雌雄各半 ,随机分为 2组 :正常对照组、烟熏组。烟熏组每天烟熏 1次 ,15天后取血测定谷丙转氨酶 ,总蛋白及白蛋白。结果 :烟熏组动物谷丙转氨酶明显高于正常对照组 (p<0 .0 5 ) ;血清总蛋白和白蛋白含量明显低于正常对照组 (p <0 .0 5 ) ;肝系数明显高于正常对照组。结论 :被动吸烟可造成大鼠肝功能的损伤     

Smoking in China: findings of the 1996 National Prevalence Survey.

CONTEXT: As the world's largest producer and consumer of tobacco products, China bears a large proportion of the global burden of smoking-related disease and may be experiencing a tobacco epidemic. OBJECTIVE: To develop an evidence-based approach supporting tobacco control initiatives in China. DESIGN AND SETTING: A population-based survey consisting of a 52-item questionnaire that included information on demographics, smoking history, smoking-related knowledge and attitudes, cessation, passive smoke exposure, and health status was administered in 145 disease surveillance points in the 30 provinces of China from March through July 1996. PARTICIPANTS: A nationally representative random sample of 128766 persons aged 15 to 69 years were asked to participate; 120298 (93.8%) provided data and were included in the final analysis. About two thirds of those sampled were from rural areas and one third were from urban areas. MAIN OUTCOME MEASURES: Current smoking patterns and attitudes; changes in smoking patterns and attitudes compared with results of a previous national survey conducted in 1984. RESULTS: A total of 41187 respondents smoked at least 1 cigarette per day, accounting for 34.1% of the total number of respondents, an increase of 3.4 percentage points since 1984. Current smoking continues to be prevalent among more men (63%) than women (3.8%). Age at smoking initiation declined by about 3 years for both men and women (from 28 to 25 years). Only a minority of smokers recognized that lung cancer (36%) and heart disease (4%) can be caused by smoking. Of the nonsmokers, 53.5% were exposed to environmental tobacco smoke at least 15 minutes per day on more than 1 day per week. Respondents were generally supportive of tobacco control measures. CONCLUSION: The high rates of smoking in men found in this study signal an urgent need for smoking prevention and cessation efforts; tobacco control initiatives are needed to maintain or decrease the currently low smoking prevalence in women.     

Cigarette smoking and urinary organic sulfides

In order to observe how cigarette smoking influences levels of thio-thiazolidine-4-carboxylic acid(TTCA),high performance liquid chromatography(HPLC) was used to detect TTCA in urine from 18 healthy male volunteers.At the sme time,the total amout of urinary organic sulfides was determined by the iodine azide test(IAT).Nine of the volunteers had smoking higtories(5 to 10 cigarettes per day,as the smoking group),and the rest only occasionally smoke (1 to 2 cigarettes per month,as the control group).Samples were collected in the early morning (limosis)and 90 minutes after smoking a cigarette.Results showed that smoking a single cigaretter could elevate the level of urinary organic sulfides both in the smoking and control groups,while a smoking habit appeared to have no significant influence on the urinary organic sulfide level.No significant cumulative effect of cigarette smoking on urinary organic sulfides was found,The influence of cigarette on uinary organic sulfides was temporary.The results suggest that cigaretter smoking might be a confounding factor in biomontoring the levels of carbon disulfide in exposed workers.