庆大霉素-肺表面活性物质磷脂乳剂气道滴入治疗大鼠克雷白杆菌性肺炎

目的　了解庆大霉素 肺表面活性物质磷脂乳剂气道滴入给药在大鼠细菌性肺炎早期的疗效。方法　将肺炎克雷白杆菌经大鼠气道滴入 ,经气道给予庆大霉素 肺表面活性物质磷脂乳剂 ;观察肺通气换气功能、肺病理形态、肺组织及循环血液中细菌数量变化及庆大霉素浓度。结果　庆大霉素磷脂乳剂气道内给药可改善氧合 ,减少肺内细菌数量 ,减轻肺部炎症病变。与静脉内用药相比 ,可获得较高的组织内药物浓度 ,并对肺通气换气功能无不良影响。结论　庆大霉素磷脂乳剂气道给药可有效治疗实验性细菌性肺炎 ,但不对肺呼吸力学产生不良影响     

庆大霉素-肺表面活性物质磷脂乳剂气道

目的：了解庆大霉素－肺表面活性物质磷脂乳剂气道滴入给药大鼠细菌性肺炎早期的疗效,方法：将肺炎克雷白 菌经大鼠气道滴入,经气道给予庆庆大霉素－肺表面活性物质磷脂乳剂;观察肺通气换气功能,肺病理形态,肺组织及循不血液中细菌数量变化及大庆霉素浓度。结果：庆大霉素磷脂乳剂气道内给药可改善氧合,减少肺内细菌数量,减轻肺部炎症病变。与静脉内用药相比,可获得较高的组织内药物浓度,并对肺通气换气功能无不良影响,结论：庆大霉素磷脂乳剂气道给药可有效治疗实验性细菌性肺炎,但不对肺呼吸力学产生不良影响。     

肺表面活性物质稀释剂延迟肺灌洗治疗烟雾吸入性损伤

目的 探讨外源性肺表面活性物质(PS)稀释剂延迟肺灌洗对大鼠严重烟雾吸入伤后内源性PS功能障碍和急性呼吸衰竭的治疗效果.方法 90只Wistar大鼠随机分为5组:Ⅰ组,正常对照(n=14);Ⅱ组,烟雾吸入(n=27);Ⅲ组,烟雾+PS灌洗+机械通气(MV),n=21;Ⅳ组,烟雾+盐水灌洗+MV,n=10;V组,烟雾+MV,n=18.伤后2 h经气管插管注入含PS(100ms/ks)的等渗盐水30 ml/kg或等量盐水行肺灌洗,MV 4 h,观察24 h;检测动脉血气、肺水量、静态肺顺应性(Cst)、支气管肺泡灌洗液(BAIF)蛋白含量、BALF表面张力特性和24 h病死率等.结果 致伤动物伤后立即出现严重缺氧和一氧化碳中毒;Ⅱ组发生急性呼吸衰竭、高通透性肺水肿和PS功能障碍;Ⅲ组Cst和BALF表面张力特性显著改善(P<0.05),但氧合能力、肺水量和BALF蛋白含量无明显好转(P>0.05).Ⅳ、V组疗效不佳.结论 外源性PS稀释剂延迟肺灌洗可一定程度恢复烟雾吸入所致内源性PS功能抑制,改善肺功能,但不能显著减轻高通透性肺水肿和呼吸衰竭,不能降低早期病死率.     

肺表面活性物质对大鼠肺内源性急性肺损伤的作用

目的观察外源性肺表面活性物质对大肠杆菌(E.coli)导致的大鼠急性肺损伤(ALI)的作用。方法设立正常大鼠组(N组)和3个实验组[E.coli导致的ALI大鼠PaO2FiO2<200mmHg(1mmHg=0.133kPa)]:对照组(C组,不用药)、表面活性物质组(PS组,经气管插管滴入CurosurfR2ml kg,160mg kg)、生理盐水组(NS组,经气管插管滴入NS,2ml kg)。每30min检测血气、胸肺有效动态顺应性,180min结束实验,进行肺病理检查,测肺指数、支气管肺泡灌洗液(BALF)蛋白含量和TNFα浓度。结果①PS组各时点PaO2较给药前升高约70%,与C组、NS组比较明显升高(P<0.05);②PS组PaCO2、pH以及胸肺有效动态顺应性各时点好于NS组(P<0.05);③PS组肺指数明显低于C组[(0.38±0.05)%对(0.43±0.05)%,P<0.05]和NS组[(0.47±0.06)%,P<0.01];④PS组肺透明膜形成较NS组减少(P<0.05),较C组有减少趋势(P=0.055);⑤PS组BALF蛋白含量明显低于C组[(0.63±0.30)mg ml对(0.96±0.25)mg ml,P<0.05]和NS组[(1.03±0.27)mg ml,P<0.01];TNFα浓度明显低于NS组[(0.35±0.23)ng ml对(2.14±1.02)ng ml,P<0.01],较C组(0.61±0.28)ng ml有减低趋势(P>0.05)。结论肺表面活性物质对E.coli所致的大鼠肺内源性ALI有治疗作用,可改善氧合,减轻肺水肿,并有减少肺透明膜形成和TNFα释放趋势。     

肺表面活性物质在哮喘中的地位

人们首先在新生儿呼吸窘迫综合症 (ＮＲＤＳ)和急性呼吸窘迫综合症 (ＡＲＤＳ)中发现了肺表面活性物质 (ｐｕｌｍｏｎａｒｙｓｕｒｆａｃｔａｎｔ,ＰＳ)量的不足和功能失常 ,使用ＰＳ替代疗法在这些疾病的临床治疗上也已取得了重大进展 ,但对其与支气管哮喘的关系则了解甚少。近 10年来 ,越来越多的证据表明 ,哮喘患者体内也存在ＰＳ量的不足和功能的异常 ,并与哮喘的发作密切相关 ,因而成为哮喘研究的一个新热点。现就ＰＳ近年来的研究进展以及在哮喘中的意义作一综述。1　ＰＳ的组成及功能ＰＳ是一种具有高度表面活性的复合磷脂 ,由 90 %…     

肺表面活性物质治疗早产儿肺透明膜病的护理

应用外源性肺表面活性物质治疗早产儿严重肺透明膜病１０例，均取得较好的效果。药液（２００ｍｇ／ｋｇ）通过气管插管及导管分４次注入气管内，并通过正压通气使均匀分布于两肺气道。为确保安全、有效，注药前必须保持气管插管及导管的良好位置，并吸清痰液。用药后６小时内不作气管内吸引。持续监测生命体征，早期发现和处理可能发生的不良反应，并及时调整呼吸机参数以避免氧中毒和气压伤。     

肺表面活性物质相关蛋白的代谢研究进展

肺表面活性物质相关蛋白主要由肺泡Ⅱ型细胞和Ｃｌａｒａ细胞合成，结过复杂的加工与修饰后分泌入气道，以维持肺表面活性物质系统结构和功能的完整性，被利用后的这些蛋白主要由Ⅱ型细胞和肺泡巨噬细胞清除。     

肺表面活性物质治疗早产儿肺透明膜病的临床研究

目的:探讨肺表面活性物质(PS)治疗早产儿肺透明膜病(HMD)的疗效及临床价值。方法:对32例诊断肺透明膜病的早产儿采用气管内快速注入PS,观察使用PS前后的动脉血气变化及机械通气情况。结果:应用PS后患儿皮肤颜色迅速转红,使用PS前后PaO2、PaCO2、pH比较差异显著,23例HMD胸片Ⅰ级、Ⅱ级及2例Ⅲ级患儿只需采用持续气道正压通气、面罩等呼吸支持和氧疗技术,7例Ⅲ级患儿机械通气。治愈率96.88%。结论:PS能有效地改善HMD患儿肺顺应性和氧合功能,缩短机械通气时间,提高治愈率。     

肺表面活性物质治疗新生儿肺透明膜病的护理

新生儿肺透明膜病 (HMD)又称新生儿呼吸窘迫综合征 (NRDS) ,主要发生于早产儿 ,胎龄愈小发病率愈高 ,其发病原因与缺乏肺泡表面活性物质 (PS)有关 ,临床上以进行性呼吸困难为主要表现[1] 。我院新生儿科 1999年 1月起采用PS替代治疗法治疗HMD ,效果满意 ,现将护理体会报告如下。1　对象与方法1 1　对象　我院新生儿科 1999年 1月～ 2 0 0 2年 10月收治的患儿 30例 ,其中 ,男 2 1例 ,女 9例 ,胎龄2 7 4周～ 34周 ,日龄 0 5h～ 8 5h ,出生体重 14 80g～ 2 2 0 0g。1 2　方法1 2 1　给药时间　患儿入院后一经确诊为HMD即应给予PS治疗…     

肺表面活性物质治疗早产儿肺透明膜病的护理

应用外源性肺表面活性物质治疗早产儿严重肺透明膜病１０例，均取得以好的效果。药液（２００ｍｇ／ｋｇ）通过气管插管及导骨分４次注入气管内，并通过正压通气使之均匀分布于两肺气道。为确保安全、有效，注药前必须保持气管插管及导管的良好位置，并吸清痰液。用药后６小时内不作气管内吸引。持续监测生命体征，早期发现和处理可能发生的不良反应，并及时调整呼吸机参数以避免氧中毒和气压伤。     

Pulmonary surfactant in patients with Pneumocystis pneumonia and acquired immunodeficiency syndrome

OBJECTIVE: Pneumocystis pneumonia (PCP) is a severe infection of the immunocompromised host, resulting in diffuse alveolar damage and life-threatening respiratory failure. We analyzed pulmonary surfactant composition and function in bronchoalveolar lavage fluid (BALF) from ventilated and spontaneously breathing HIV-positive patients with PCP. DESIGN: Prospective clinical trial. SETTING: University hospital intensive care unit. PATIENTS: Thirty-four spontaneously breathing (SB-PCP) and 20 ventilated HIV-positive patients with PCP (V-PCP), ten patients with acute respiratory distress syndrome (ARDS), 11 spontaneously breathing patients with bacterial pneumonia (PNEU), and 22 healthy volunteers. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Total phospholipid in BALF did not differ between any category vs. controls, whereas total protein increased approximately 14-fold in V-PCP and five-fold in SB-PCP compared with controls (p < .001). The relative content of large surfactant aggregates (LA) was reduced in SB-PCP and V-PCP compared with controls (p < .05). The phospholipid and fatty acid profiles showed a significant reduction in the relative content of phosphatidylcholine (PC), phosphatidylglycerol, and palmitic acid in PC in all patient categories compared with controls, with more in V-PCP (p < .001) compared with SB-PCP (p < .05). The neutral lipid-to-phospholipid ratio in LA was three-fold elevated in V-PCP (p < .01 compared with control) but not in SB-PCP. Analysis of neutral lipid classes showed a significant increase in the relative content of triglycerides and a reduction in free fatty acids in V-PCP compared with controls. BALF surfactant protein (SP)-A and SP-D significantly increased in V-PCP and SB-PCP, but not in ARDS and PNEU, compared with controls (p < .05). SP-B and SP-C content in LA remained unchanged in PCP compared with controls but decreased significantly in ARDS and PNEU. The minimum surface tension of LA was impaired (p < .001) in V-PCP more than in SB-PCP and was strongly correlated with the reduction in palmitic acid levels in PC LA (r = -.81). Reductions in phosphatidylglycerol strongly correlated with decreased Pao2/Fio2 values (r = .72). CONCLUSIONS: We conclude that severe alterations in surfactant function and composition occur in patients with PCP and are even more pronounced in ventilated patients than in nonventilated patients. Surfactant lipid changes in PCP, but not surfactant protein profiles, closely resemble those found in ARDS.     

Pulmonary surfactant: functions, abnormalities and therapeutic options

The first successful clinical pilot studies of surfactant replacement were published about 20 years ago as a logical extension of experimental studies showing beneficial effects in pre-term animals. The efficacy of this therapy for immature new-borns has been confirmed in various controlled trials and surfactant therapy is now part of the routine management of the infant respiratory distress syndrome. During the last decade there has been growing insight into the functional role of surfactant components and the mechanisms by which exogenous surfactant exerts its therapeutic effects on lung mechanics, gas exchange and host defence. Of particular interest in this context is the essential role that surfactant-associated proteins play in the surface tension-limiting ability of surfactant, as well as their contribution to pulmonary defence. Indications for surfactant replacement have widened in recent years and promising results have been obtained for adult conditions such as the acute respiratory distress syndrome (ARDS), pneumonia, chronic obstructive and allergic lung diseases. This review outlines the complexity of the surfactant system and describes its basic biophysics, physiology and biochemistry. Problems related to the development of exogenous surfactant preparations, the exploration of clinical targets for surfactant therapy and pathophysiological mechanisms interfering with surfactant function in various forms of lung disease will be discussed.     

Effect of surfactant replacement onPneumocystis carinii pneumonia in rats

The effect of intratracheal surfactant instillation on pulmonary function in rats withPneumocystis carinii pneumonia (PCP) was investigated. In those animals which developed PCP with severe respiratory failure after administration of cortisone acetate s. c. over 8–12 weeks, pulmonary function was improved by surfactant instillation. PaO₂ values 30 min after surfactant instillation were significantly higher compared to pretreatment values and also compared to PaO₂ values of rats 30 min after receiving saline (482.9 mmHg±44.7, 170.7 mmHg ±39.3 and 67.2 mmHg±17.4, respectively). Histological examination showed that alveoli of rats with PCP which received no exogenous surfactant are filled with foamy edema, whereas after exogenous surfactant alveoli are stabilized and well-aerated. These results indicate that exogenous surfactant may help patients with severe PCP to overcome an acute stage of respiratory distress.This work was financially supported, in part, by The Dutch Foundation for Medical Research (SFMO)