Effect of ipratropium bromide on airway and pulmonary muscarinic receptors in a rat model of chronic obstructive pulmonary disease

Objective　To observe the level of muscarinic receptors in airway and lung tissues, and the effect of inhaled ipratropium bromide on these receptors in a rat model of chronic obstructive pulmonary disease (COPD). Methods　This model was developed by exposure of rats to 250 ppm SO2 gas, 5?h/d, 5d/wk, for a period of 7 wk. The COPD rats inhaled 0.025% aerosolized iratropium bromide for 20 min, 2 times daily, in an airtight chamber. Muscarinic receptors in airway and lung tissues of normal rats, ipratropium bromide-treated COPD rats and the recovering COPD rats were measured by the radio-ligand binding assay. Results　Airway/lung pathology and pulmonary function tests showed that chronic SO2 exposure caused pathophysiologic changes similar to those observed in human COPD. The density (0.038±0.011, pmol/mg protein) and affinity (Kd, 23±11 pmol/L) of muscarinic receptors in airway and lung tissues of COPD rats were not changed compared with those of normal control rats (0.030±0.008 and 29±19, respectively, P>0.05). Densities of the muscarinic receptors were not changed after inhalation of ipratropium bromide for 5 days, but increased significantly after inhalation for 30 days, as compared with those of the untreated COPD rats. The muscarinic receptors returned the normal levels at day 6 after cessation of ipratropium bromide treatment. There were no differences among different groups of rats in equilibrium dissociation constants (Kd). Conclusion　A rat model of COPD with pathophysiologic changes similar to the human counterpart was developed using chronic SO2 exposure. There was no significant change in the number and function of muscarinic receptors in airway and lung tissues of the COPD rats, but upregulation of the muscarinic receptors was observed after long-term inhalation of ipratropium bromide.     

海水淹溺肺水肿兔血浆MDA和SOD的变化

目的 :观察海水淹溺肺水肿 (PE SWD)兔血浆中丙二醛 (MDA)和超氧化物歧化酶 (SOD)变化规律 ,探讨上述两项指标发生变化的原因和机制。方法 :用核黄素光照法和硫代巴比妥酸法 ,对PE SWD兔动脉血浆MDA和SOD进行定量检测和动态观察。结果 :灌海水后 30min ,MDA和SOD较灌海水前均显著升高 ,尔后两者均逐渐下降 ,但仍远远高于灌海水前。结论 :PE SWD发生发展过程中 ,MDA的损害性作用使肺泡表面活性物质表面特性发生改变 ,影响了正常的呼吸功能 ,并掩盖了SOD的保护性作用。     

川芎嗪与前列腺素E1联合治疗慢性肺源性心脏病急性发作期疗效观察

目的 观察联用川芎嗪（ＬＴ）和前列素（ＰＧＥ４）治疗慢性肺源性心脏病（肺心病）急性发作期患者的临床疗效。方法 １０５例肺心病急性发作期患者随机分为治疗组（５４例）和对照组（５１例）,治疗组采用ＬＴ联合ＰＧＥ１治疗;对照组采用单纯ＰＧＥ１治疗。２组患者于治疗后１０ｄ测定血液流变学指标并进行疗效判定。结果 治疗组显效率（５９．２６％）明显高于对照组（３９．２２％）,２组比较具有显著差异（Ｐ〈０．０５）     

低氧对体外培养的肺血管周细胞免疫表型的影响

用细胞培养、免疫细胞化学染色、图像分析及流式细胞术观察低氧和猪肺动脉缺氧内皮细胞条件培养液(HECCM)对体外培养的新生大鼠肺血管周细胞 (PC)α- SM- actin、 CD34 、 S- 10 0和 PCNA的表达及细胞周期的影响。结果发现 ,低氧和 HECCM可促进 PC表达α- SM- actin和 PCNA,而抑制 CD34 和 S- 10 0的合成 ,促进 PC由静止期 (G0 /G1 期 )进入 DNA合成期 (S期 )及有丝分裂期 (G2 M期 )。提示 ,低氧不仅能促进 PC增殖 ,而且还可促进其向平滑肌样细胞转化。故 PC是慢性低氧性肺动脉高压时无肌型细动脉肌化的重要细胞来源。     

99mTc-DTPA气溶胶显像测定呼吸道粘液纤毛清除功能

为进一步研究呼吸道疾病时的粘液纤毛清除功能,采用99mTc-DTPA气溶胶吸入显像,通过电影显示定性和定量指标分析.对18 例健康受试者和患者进行了显像研究,得到气道清除率和粘液纤毛清除率的正常值,并观察了32例慢性阻塞性肺病(COPD)患者气管-支气管纤毛清除功能的改变.结果显示,健康受试者与COPD患者粘液纤毛清除率(mm/min)分别为3.89±0.92和1.32±0.59,两者比较有显著性差异(P＜0.01),COPD患者不同时间气道清除率和粘液纤毛清除率均明显低于健康受试者(P＜0.01).本研究方法简便客观,具有定性观察和定量分析的优点,对于呼吸系统其它疾病(如支气管扩张、原发性纤毛无运动)的研究及药物疗效的评价具有重要的临床实用价值.     

慢性阻塞性肺病胸腔镜肺减容手术的治疗观察

目的 评价胸腔镜肺减容手术对重度慢性肺病的治疗疗效和病情改善情况。方法 对我院１０例重度慢性阻塞性肺病患者行肺减容手术后随访１年半观察,同时与１０例未做手术的重度ＣＯＰＤ患者比较,比较其在入院次数,肺功能改善情况（自行上楼比较）、吸氧时间、生活自理能力等方面的差异。结果 手术组病人因慢性支气管炎急性发作、肺部感染再次入院次数明显减少,自行上楼气急明显比手术前减轻,吸氧时间明显减少,、生活自理能力增     

综合医院确诊的39例肺结核患者转诊结果随访调查

目的;了解并评价综合医院内科确诊的活动性肺结核病例转诊结果。方法：对我院呼吸内科１９９５年８月－１９９８年８月确认的３９例活动性肺结核患者（不包括结核性胸膜炎）转往结构防治专业机构的结果进行信访和电话随访。结果：仍的３９例活动性肺结核患者中有３５例在确诊后１周内结核病接受０．５ａ－１ａ的全地化疗,３３例获得良好效果,２例死亡,死因分别为肺间质纤维化合并感染肺心病及呼吸衰竭。３例慢性纤维空洞型肺结核     

Characterization of α1-adrenoceptor subtypes mediating contractions to phenylephrine in rat thoracic aorta,mesenteric artery and pulmonary artery

1. The subtype of α₁-adrenoceptor mediating contractions to phenylephrine of the rat thoracic aorta, mesenteric artery and pulmonary artery were investigated by use of antagonists which show selectivity between the cloned α₁-adrenoceptor subtypes in binding studies.
2. Cumulative concentration-contraction curves for phenylephrine were competitively antagonized in the rat thoracic aorta by prazosin (pA₂ 9.9), WB4101 (pA₂ 9.6), 5-methylurapidil (pA₂ 8.1), benoxathian (pA₂ 9.2) and indoramin (pA₂ 7.4). These compounds were also competitive antagonists in the mesenteric and pulmonary arteries (except for 5-methylurapidil in the pulmonary artery), (prazosin pA₂ 9.9 and 9.7; WB4101 pA₂ 9.8 and 9.6; 5-methylurapidil pA₂ 7.9 and pK_B estimate 8.0; benoxathian pA₂ 8.8 and 9.3; indoramin pA₂ 7.2 and 7.5, respectively).
3. RS 17053 was not a competitive antagonist in any blood vessel as Schild plot slopes were greater than unity. The pK_B estimates for RS 17053 were 7.1 in aorta, 7.0 in the mesenteric artery and 7.7 in the pulmonary artery.
4. The α_1D-subtype selective antagonist BMY 7378 appeared to be non-competitive with shallow Schild plot slopes. The data were better fitted with two lines in all tissues, with Schild plot slopes that were no longer different from unity, except in the pulmonary artery. The higher affinity site for BMY 7378 in the aorta had a pA₂ of 9.0, while it was 8.8 and 8.9 in the mesenteric and pulmonary arteries, respectively.
5. MDL73005EF acted in a non-competitive manner in all three blood vessels, with shallow Schild plot slopes. The pK_B estimates for MDL73005EF were 8.4 in aorta, 7.5 in the mesenteric artery and 8.0 in the pulmonary artery.
6. In all three blood vessels the functionally determined antagonist affinity estimates correlated best with published pK_i values for their displacement of [³H]-prazosin binding on membranes expressing cloned α_1d-adrenoceptors compared with α_1a- or α_1b-adrenoceptors. The antagonist affinity estimates in the aorta, mesenteric and pulmonary arteries correlated highly with their previously published pA₂ values in rat aorta (α_1D) and less well with those for α_1A- and α_1B-adrenoceptors mediating contraction of the rat epididymal vas deferens and rat spleen, respectively.
7. The results of this study suggest that the contraction to phenylephrine of the rat thoracic aorta, mesenteric artery and pulmonary artery are mediated in part via the α_1D-subtype of adrenoceptor. The data for both BMY 7378 and MDL73005EF in all three blood vessels are consistent with receptor heterogeneity. However, the identity of the second site is unclear.

     

Pulmonary venous flow as assessed by Doppler echocardiography: potential clinical applications

During the past few years Doppler assessment of pulmonary venous flow has gained increasing interest. The growing experience with the use of transesophageal echocardiography, the approach that nearly always yields registrations adequate for quantitative analysis, has markedly contributed in this respect. The Doppler-derived pulmonary venous flow pattern can be regarded as a measure of left atrial inflow and it augments the clinical significance of Doppler transmitral flow in the evaluation of diastolic left ventricular function. This article summarizes physiological background, possible applications, and limitations of Doppler echocardiography of pulmonary venous flow in clinical cardiology.     

潜艇常见气体对离体细胞化学发光的影响

目的 :用化学发光法检测O2 、CO2 、CO和正庚烷 (CxHy)四种气体对离体家兔肺泡巨噬细胞 (AM )的直接效应。 方法 :将AM悬液暴露于上述气体 ,不同时间检测用PMA激发的细胞发光及其存活率。结果 :培养在 99.5 %N2 (0 .5 %O2 )中的AM受激发光仅能维持 10h ;高浓度O2 、CO2 、CO和CxHy具有刺激或增强AM发光之效应 ;含 16 %O2 、1.9%CO2 、46mg/m3 CO和 176mg/m3 CxHy的模拟潜艇混合气体未见对AM激发光功能和存活率产生不利影响。结论 :空气氧含量对细胞十分重要 ,提高氧浓度有利于细胞存活 ,但氧浓度 >16 %和 <2 0 %的低氧还原性气体环境更有利细胞长时间生存。