Inhaled iron, unlike manganese, is not transported to the rat brain via the olfactory pathway

Iron and manganese share structural, biochemical, and physiological similarities. The objective of this study was to determine whether iron, like manganese, is transported to the rat brain via the olfactory tract following inhalation exposure. Eight-week-old male CD rats were exposed to approximately 0.31 mg Fe per m(3) (mass median aerodynamic diameter = 2.99 microm; geometric standard deviation = 1.15) via inhalation for a target duration of 90 min. Following exposure, rats were euthanized immediately (0) or at 1, 2, 4, 8, or 21 days postexposure. In addition to nasal and regional brain tissues, blood, and viscera were also collected. 59Fe concentrations were determined by gamma spectrometry. Further, heads were collected and frozen, and autoradiograms were prepared to visualize the location of 59Fe from the nose to the brain. Finally, olfactory mucosa samples collected at 0, 2, 4, and 21 days postexposure were further analyzed using high-performance liquid chromatography (HPLC) plus gamma spectroscopy to determine the association between 59Fe and transferrin. Data obtained from gamma spectrometry revealed that most of the iron remained in the nasal regions of the olfactory system and that less than 4% of iron deposited on the olfactory mucosa was observed in the olfactory bulb. Autoradiograms confirmed the data obtained from gamma spectrometry. 59Fe activity was absent in the olfactory regions of the brain even 4 days postexposure. Further, HPLC-gamma spectroscopy analyses indicated that 59Fe in the olfactory mucosa was coeluted with transferrin. Hence iron, unlike manganese, is not readily transported to the brain via the olfactory tract.     

Carcinogenicity assays of wood dust and wood additives in rats exposed by long-term inhalation

Objective: This study evaluates whether wood dust and/or wood preservatives develop a carcinogenic potential against the tissues of the airways of rats. Methods: The formation of tumors of the respiratory tract after exposure to wood dust was studied in six groups of approximately 60 female Fischer 344 rats exposed by long-term inhalation to mean concentrations of (1) 18 mg/m³ of untreated oak wood dust, (2) wood preservatives containing ca. 1 μg/m³ lindane and 0.2 μg/m³ of pentachlorophenol (PCP) in the exposure air, or lindane and 18 μg/m3 of PCP (group lindane/PCP vapors, and group oak wood treated with lindane/PCP), (3) 21 or 39 μg/m³ of sodium dichromate (calculated as CrO₃, group chromate aerosol and group oak wood with chromate), and 72 μg/m³ of N-nitrosodimethylamine vapors as positive control. The negative control group consisted of 115 animals (sham-exposed). Results: Tumors of the nasal cavity developed in two rats exposed to chromate aerosol or in combination with wood dust (2/102, 2%). Malignant tumors of the lower respiratory tract were induced only in exposed groups of rats (three adenocarcinomas of the lung and four bronchiolar lung carcinomas, 7/254, 2.8%). More respiratory tract tumors were observed in rats exposed to chromate or wood with chromate (5/102, 5%), also in groups exposed to oak wood dust (oak untreated, oak + chromate, oak + lindane/PCP; together 5/155, 3.2%). Analysis of `unpreserved' oak wood dust revealed up to 5 μg/m³ of chromate. When this exposure was taken into account, eight of nine animals with respiratory tract tumors (including nasal cavity) had exposure to chromate, while only one tumor occurred in the group lindane/PCP. Otherwise the incidence of systemic tumors was increased in animals exposed to lindane/PCP, due in particular to a significantly increased incidence of liver tumors (OR=3.7; 1.24–11.3; P=0.019). Fatal (mucoepidermoid) tumors were induced by N-nitrosodimethylamine (NDMA) in the positive control (14/46, 30%). No such tumors of the respiratory tract were observed in the negative control. Conclusions: Tumors in the respiratory tract were found only in exposed animals, predominantly in the groups which inhaled oak wood dust and chromate stain. Chromate may play a decisive role for the etiology of tumors of the nasal cavity in wood workers. This assumption should be supported by further dose-response studies. Received: 23 May 2000 / Accepted: 13 September 2000     

布地奈德、沙丁胺醇雾化吸入治疗儿童哮喘急性发作的疗效观察

目的:观察布地奈德、沙丁胺醇雾化吸入对儿童哮喘急性发作的临床疗效。方法:将136例哮喘患儿随机分为两组,对照组64例,采用氨茶碱、琥珀酸氢化可的松等静滴,解痉、平喘及吸氧等对症治疗,合并感染者使用抗生素;观察组72例,在对照组治疗的基础上加用布地奈德、沙丁胺醇雾化吸入,每日3次,每次5~10min。结果:观察组的主要临床表现恢复正常的时间较对照组短,控制率较高,两组差异均有显著性(P<0.01)。结论:布地奈德、沙丁胺醇雾化吸入可作为治疗儿童哮喘急性发作的有效方法。     

雾化吸入肺表面活性物质治疗新生儿呼吸窘迫综合征的临床研究

目的:观察雾化吸入肺表面活性物质(Pulmonary surfactant,PS)治疗新生儿呼吸窘迫综合征(Neonatal respir-atory distress syndrome,NRDS)的临床效果。方法:44例NRDS患儿分为3组,分别雾化吸入PS(雾化组)16例,用气道内滴入PS(气内组)16例以及单纯应用呼吸机治疗(单纯组)12例。观察3组患儿不同方法治疗后的临床症状,动脉血气分析,上机时间以及并发症情况。结果:雾化组中,治疗后仅3例需要机械通气,上机时间0～52h,平均上机时间(45.3±8.33)h,治疗后动脉血气(PH、PO2、PCO2、a/APO2)结果均有改善,显效12例,有效4例,并发肺部感染2例;气内组中有9例需机械通气,平均上机时间(76±8)h,显效13例,有效3例,并发肺部感染10例,肺不张2例;单纯组12例中,均需应用呼吸机辅助通气,平均上机时间(105±15)h,显效6例,有效5例,无效1例,并发肺部感染11例,气胸1例,肺不张2例。结论:雾化吸入PS能在较短时间有效改善肺换气和弥散功能,促进氧合,改善临床症状,减少并发症,减少上呼吸机时间。     

七氟醚吸入麻醉在小儿唇腭裂手术中的应用

目的观察七氟醚吸入麻醉用于小儿唇腭裂手术的麻醉诱导、维持及苏醒的临床效果。方法50例唇腭裂患者，ASAⅠ-Ⅱ，年龄2月-12岁。6岁以下患儿采用七氟醚快速吸入麻醉诱导，七氟醚5—8vd％＋吸入氧6L／min，待疼痛消失后，经口异型管（oral）气管插管；6岁以上患儿静注芬太尼1μg／kg，同时吸入七氟醚5—8vol％＋吸入氧6L／min，待疼痛消失后，经口异型管（oral）气管插管或喉罩（LMA）置入，待麻醉诱导完毕，术者做眶下神经阻滞。术中七氟醚维持2—3vol％，＋吸入氧1-3L／min，保持患者自主呼吸存在。记录睫毛反射消失时间，疼痛反射消失时间，术后苏醒时间，观察幼儿是否合作，诱导期患儿是否合作，有无咳嗽、屏气及喉痉挛，有无术后躁动及恶心呕吐等并发症。记录诱导前、睫毛反射消失时、气管插管时、术中、术毕各时间点MAP、HR、SpO2％、PETCO2的变化。结果睫毛反射消失时间（48．5±13．5）s，疼痛反射消失（147±23．5）s苏醒时间（3．82±1．25）min。6岁以上患儿中2例术中体动，追加异丙酚0．5mg／kg后麻醉平稳。无一例术后恶心呕吐及躁动。插管时MAP和HR稍有增快，插管后恢复诱导前水平，SpO2、PETCO2均无显著改变。结论七氟醚具有气味芬芳，诱导迅速，术中可不需肌松弛剂，麻醉维持平稳，苏醒快，不良反应少，是理想的吸入麻醉剂。     

重度吸入性损伤的早期救治

目的探讨重度吸入性损伤早期救治的方法。方法对29例重度吸入性损伤患者实施"四早"救治方案,即:早期气管切开;早期充分给氧;早期气道湿化、灌洗;早期纤维支气管镜检查及治疗。结果重度吸入性损伤患者应用"四早"救治方案后,显著地提高了救治的成功率。结论对重度吸入性损伤患者按"四早"方案进行救治是有效可行的。     

Comparison of Salmeterol with Beclomethasone in Adult Patients with Mild Persistent Asthma Who Are Already on Low-Dose Inhaled Steroids

Current guidelines on asthma management recommend the early use of inhaled corticosteroids. Recent studies of patients with moderate to severe asthma show that the addition of salmeterol is superior to a further increase of the steroids. In this study with adult, mild persistent asthma patients, we compared the effects of adding salmeterol 50 μg b.i.d. versus beclomethasone dipropionate (BDP) 200 μg b.i.d. (both via Diskhaler dry powder inhaler) to the low-dose inhaled steroids. A double-blind, randomized, parallel-group study was conducted with a run-in period of 2 weeks and a treatment period of 12 weeks. Patients (n = 233) were randomized with a peak expiratory flow (PEF) reversibility of 22 10% (mean ± SD) in the run-in period. The morning PEF was 84 ± 17% predicted and the age was 42 ± 14 years (45% males). The average prestudy inhaled steroid dose was 361 μg daily. Within a week of salmeterol treatment the daily PEF recordings reached maximal levels. At the end of the treatment period the evening PEF remained significantly better in the salmeterol group than in the BDP group (p = 0.036). The PEFs, measured at the general practitioners (GPs) office, were at least 95% of the predicted values and the post-salbutamol values at the end of both treatments. However, the salmeterol group had already obtained this level after 2 weeks and differed significantly from the beclomethasone group (p = 0.003 for percent predicted and p = 0.0007 for post-salbutamol PEF values). The symptom scores and the use of rescue medication showed a similar profile. Quality of life improved with both treatments, but without significant statistical differences between the groups. The frequency of adverse events, typical for beta 2-agonists, was low and showed no differences between the groups. These results showed that the addition of salmeterol is at least as effective as adding beclomethasone in normalizing peak flows and improving asthma control in mild persistent asthma patients. Furthermore, salmeterol has a much faster onset of action.     

联合博利康尼和布地奈德雾化吸入治疗哮喘急性发作的临床疗效分析

目的联合博利康尼、布地奈德雾化吸入在哮喘急性发作时的治疗效果。方法对60例哮喘急性发作期患者做疗效对比。结果哮喘急性发作时,联合博利康尼、布地奈德雾化吸入疗效优于常规治疗。急性发作期雾化吸入治疗效果满意（P〈0.01）。结论肾上腺素β2受体激动剂与糖皮质激素联合雾化吸入是控制哮喘急性发作的安全有效的方法。     

高频喷射通气对重度烧伤合并吸入性损伤患者早期的呼吸支持

目的　观察高频喷射通气 (highfrequencyjetventilation ,HFJV)对重度烧伤合并吸入性损伤患者早期的治疗作用。　方法　 2 0例重度烧伤 (TBSA 79.6 %± 2 9.3% )并吸入性损伤患者 ,其中 19例行气管切开手术 ,1例经鼻插管。为防低氧血症 ,所有患者均应用HFJV ,观察通气前和通气后 11d内血气、呼吸率和脉搏等指标的变化。　结果　气管切开时间为伤后 (2 .7± 2 .4 )d ,HFJV时间为伤后(4.4 0± 2 .9)d。HFJV后 1～ 3d ,PaO2 显著高于通气前水平 (P <0 .0 1) ,随后HFJV 1周 ,PaO2 仍维持在较高水平。在整个通气期间 ,PaCO2 、呼吸率和脉搏率均无明显变化。结论　在重度烧伤合并吸入性损伤早期 ,HFJV有利于氧合作用的改善而无明显副作用 ,是一较为适用的呼吸支持方式     

吸入一氧化氮对急性肺损伤动物氧合的影响

目的　 利用不同动物模型比较吸入NO对动物急性肺损伤氧合的影响。 方法 　应用健康雄性Wistar大鼠和新西兰兔各 14只 ,经右心导管注入油酸制成急性肺损伤模型。 结果 　油酸注入大鼠右心后 ,对照组、NO组氧分压由 ( 3 2 2 3± 3 0 2 )mmHg和 ( 3 2 2 3± 2 2 9)mmHg( 1mmHg =0 13 3kPa)降为 ( 10 1 6± 12 9)mmHg和 ( 110 9± 6 1)mmHg ,吸入 40ppmNO 1h后氧分压未有上升趋势。兔急性肺损伤时 ,对照组和NO组氧分压分别由 ( 14 7 2± 11 8)mmHg和 ( 14 3 4± 7 3 )mmHg降为 ( 84 6± 4 8)mmHg和 ( 85 1± 8 6)mmHg ,吸入 2 0 ppm、40 ppmNO上升为 ( 115 1± 10 7)mmHg和 ( 117 7± 11 9)mmHg。 结论 　轻度肺损伤时吸入NO可使氧合得到适当改善 ,提高血氧分压。