Background: Respiratory distress is one among the leading reasons cause mortality for infants especially for preterm babies or light weight babies. Surfactant therapy in premature infants can decrease mortality, duration of respiratory treatment, pulmonary air leaks and chronic lung disease. Objective: This study aims to assess the effect of surfactant therapy in premature infants with respiratory distress syndrome at Intensive Care Unit of Children Hospital N\xb0.2. Subjects and method:A cases study about premature infants less than 24 hours after birth with respiratory distress syndrome (RDS) admitted to intensive care unit and treated with surfactant from January 2007 to July 2007 at the Children Hospital No 2. There were 30 cases recruited. The data was collected and analyzed by EpiInfo software 2002.Results: Most of them improved in respiration status after using surfactant (96.7%); no case of air leak was seen; 3 bronchopulmonary dysplasia cases and 4 deaths due to nosocomial infection were seen. Conclusion: Surfactant therapy was effective in premature infants with RDS. In the case of having economic advantages, surfactant may be indicated for preventive treatment on the premature and light weigh infants without respiratory distress syndrome on clinical aspect.
Respiratory Distress Syndrome ; Newborn/ therapy ; Pulmonary Surfactant-Associated Proteins ; Infant ; Premature

OBJECTIVETo investigate the effects of maternally administered dexamethasone and ambroxol on the mRNA levels of surfactant proteins (SP-A, SP-B and SP-C) expression in fetal rat lungs at gestational age day 19.

METHODSA 19-day fetal rat lung model was employed. In situ hybridization was used to detect the expression of SP-B mRNA in alveolar type II cell, and the levels of SP-A, SP-B and SP-C mRNAs were detected by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTS(1) SP-B mRNA was detected in situ in alveolar type II cells in fetal rat lung of day 19 gestational age; (2) In the late developmental period of fetal rat lungs, alveolar type II cells were also found around bronchus; (3) Comparing to beta-actin mRNA, the relative values of SP-A, SP-B and SP-C mRNAs were 0.81 +/- 0.26, 0.97 +/- 0.20 and 0.88 +/- 0.11 in fetal lung in the control group. The relative values of mRNAs of SP-A, SP-B and SP-C to beta-actin were 1.04 +/- 0.16, 1.28 +/- 0.29, 1.09 +/- 0.25 in fetal lungs of the ambroxol injected rats, and were 1.08 +/- 0.25, 1.23 +/- 0.35, 1.21 +/- 0.25 in fetal lungs of the dexamethasone injected rats, respectively. Both ambroxol and dexamethasone-treated rats had significantly higher mRNA expression of surfactant proteins compared to the control saline injected animals (P < 0.05). (4) There were no significant differences between ambroxol and dexamethasone in the effects of increasing expressions of surfactant protein mRNAs (P > 0.05).

CONCLUSIONAntepartum administration of both ambroxol and dexamethasone can significantly increase fetal lung SP-A, SP-B and SP-C mRNAs expression.

Ambroxol ; pharmacology ; Animals ; Dexamethasone ; pharmacology ; Expectorants ; pharmacology ; Female ; Gene Expression Regulation, Developmental ; drug effects ; Glucocorticoids ; pharmacology ; Lung ; drug effects ; embryology ; metabolism ; Pregnancy ; Pulmonary Surfactant-Associated Protein A ; genetics ; Pulmonary Surfactant-Associated Protein B ; genetics ; Pulmonary Surfactant-Associated Protein C ; genetics ; Pulmonary Surfactant-Associated Proteins ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction

Respiratory distress syndrome (RDS) among preterm infants is typically due to a quantitative deficiency of pulmonary surfactant. Aside from the degree of prematurity, diverse environmental and genetic factors can affect the development of RDS. The variance of the risk of RDS in various races/ethnicities or monozygotic/dizygotic twins has suggested genetic influences on this disorder. So far, several specific mutations in genes encoding surfactant-associated molecules have confirmed this. Specific genetic variants contributing to the regulation of pulmonary development, its structure and function, or the inflammatory response could be candidate risk factors for the development of RDS. This review summarizes the background that suggests the genetic predisposition of RDS, the identified mutations, and candidate genetic polymorphisms of pulmonary surfactant proteins associated with RDS.
Genetic Predisposition to Disease ; Humans ; Infant, Newborn ; Infant, Premature ; Polymorphism, Genetic ; Pulmonary Surfactant-Associated Proteins ; Pulmonary Surfactants ; Risk Factors* ; Twins

Pulmonary surfactant ( PS ) compromises lipids and surfactant proteins (SP) and lines on the alveolar air-liquid interface. It can reduce surface tension, prevent alveoli from collapse and reduce alveoli edema by disaturated dipalmitoylphosphatidylcholine. It also modulates the pulmonary immunology by SP-A and SP-D. In this study,we established a rat model of immunocompromised host (ICH) with pulmonary infection of Pseudomonas aeruginosa (P. aeruginosa), then studied its pulmonary inflammatory reaction and analyzed the concentration of lipids and SP-A in bronchoalveolar lavage fluid (BALF) during infection.
Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; microbiology ; Lipids ; analysis ; Lung ; microbiology ; Male ; Neutrophils ; physiology ; Pneumonia, Bacterial ; immunology ; metabolism ; Proteolipids ; analysis ; Pseudomonas Infections ; immunology ; metabolism ; Pulmonary Surfactant-Associated Protein A ; Pulmonary Surfactant-Associated Proteins ; Pulmonary Surfactants ; analysis ; Rats ; Rats, Sprague-Dawley

Inhalation injury is a major contributor to the morbidity and mortality associated with serious burns. The improvement in the understanding of smoke inhalation injury had been obtained in the last half century in China. The models of steam and smoke inhalation injury had been reproduced and a series of experimental studies had been performed. It was found that chemical bronchiotracheitis, pulmonary edema and alveolar collapse (atelectasis) were the primary pathologic findings after inhalation injury. The second inflammatory response would play an important role in the development of acute respiratory failure. The roles of some cytokines, inflammatory cells and pulmonary surfactants in the development of inhalation injury had been elucidated. The etiologic factors and the pathophysiologic changes in inhalation injury had been illustrated clearly. These basic science investigations had led to the advances in protective strategies for the complications of inhalation injury. Now the morbidity and mortality of inhalation injury have decreased markedly in China.
Burns, Inhalation ; etiology ; therapy ; China ; High-Frequency Ventilation ; Humans ; Pulmonary Surfactant-Associated Proteins ; Smoke Inhalation Injury ; etiology ; therapy

PURPOSE: Pulmonary surfactants for preterm infants contain mostly animal-derived surfactant proteins (SPs), which are essential for lowering surface tension. We prepared artificial pulmonary surfactants using synthetic human SP analogs and performed in vitro and in vivo experiments. MATERIALS AND METHODS: We synthesized peptide analogues that resemble human SP-B (RMLPQLVCRLVLRCSMD) and SP-C (CPVHLKRLLLLLLLLLLLLLLLL). Dipalmitoylphosphatidylcholine (DPPC), phosphatidylglycerol (PG), and palmitic acid (PA) were added and mixed in lyophilized to render powdered surfactant. Synsurf-1 was composed of DPPC:PG:PA:SP-B (75:25:10:3, w/w); Synsurf-2 was composed of DPPC:PG:PA:SP-C (75:25:10:3, w/w); and Synsurf-3 was composed of DPPC:PG:PA:SP-B:SP-C (75:25:10:3:3, w/w). We performed in vitro study to compare the physical characteristics using pulsating bubble surfactometer and modified Wilhelmy balance test. Surface spreading and adsorption test of the surfactant preparations were measured. In vivo test was performed using term and preterm rabbit pups. Pressure-volume curves were generated during the deflation phase. Histologic findings were examined. RESULTS: Pulsating bubble surfactometer readings revealed following minimum and maximum surface tension (mN/m) at 5 minutes: Surfacten® (5.5±0.4, 32.8±1.6), Synsurf-1 (16.7±0.6, 28.7±1.5), Synsurf-2 (7.9±1.0, 33.1±1.6), and Synsurf-3 (7.1±0.8, 34.5±1.0). Surface spreading rates were as follows: Surfacten® (27 mN/m), Synsurf-1 (43 mN/m), Synsurf-2 (27 mN/m), and Synsurf-3 (27 mN/m). Surface adsorption rate results were as follows: Surfacten® (28 mN/m), Synsurf-1 (35 mN/m), Synsurf-2 (29 mN/m), and Synsurf-3 (27 mN/m). The deflation curves were best for Synsurf-3; those for Synsurf-2 were better than those for Surfacten®. Synsurf-1 was the worst surfactant preparation. Microscopic examination showed the largest aerated area of the alveoli in the Synsurf-3 group, followed by Synsurf-1 and Surfacten®; Synsurf-2 was the smallest. CONCLUSION: Synsurf-3 containing both SP-B and SP-C synthetic analogs showed comparable and better efficacy than commercially used Surfacten® in lowering surface tension, pressure-volume curves, and tissue aerated area of the alveoli.
1,2-Dipalmitoylphosphatidylcholine ; Adsorption ; Animal Experimentation* ; Animals* ; Humans ; In Vitro Techniques* ; Infant, Newborn ; Infant, Premature ; Palmitic Acid ; Pulmonary Surfactant-Associated Proteins ; Pulmonary Surfactants ; Reading ; Surface Tension

Pulmonary surfactant (PS) is synthesized and secreted by alveolar epithelial type II (AEII) cells, which is a complex compound formed by proteins and lipids. Surfactant participates in a range of physiological processes such as reducing the surface tension, keeping the balance of alveolar fluid, maintaining normal alveolar morphology and conducting host defense. Genetic disorders of the surfactant homeostasis genes may result in lack of surfactant or cytotoxicity, and lead to multiple lung diseases in neonates, children and adults, including neonatal respiratory distress syndrome, interstitial pneumonia, pulmonary alveolar proteinosis, and pulmonary fibrosis. This paper has provided a review for the functions and processes of pulmonary surfactant metabolism, as well as the connection between disorders of surfactant homeostasis genes and lung diseases.
ATP-Binding Cassette Transporters ; genetics ; DNA-Binding Proteins ; genetics ; Homeostasis ; Humans ; Lung Diseases ; genetics ; Pulmonary Surfactant-Associated Protein C ; genetics ; Pulmonary Surfactants ; metabolism ; Transcription Factors

OBJECTIVETo investigate the change of lung surfactant protein (SP) A,B,C,D of rats following silica dust exposure in order to provide the evidences for the early diagnosis indices or therapy of silicosis.

METHODS60 male SD rats were randomly divided into silica group, and corresponding controls group. Rats in silica group were administrated 1 ml silica solution by intratracheal instillation at dose of 50 mg/ml. Rats in control group were administrated the same amount saline. At 3rd, 7th, 14th, 21st, 28th after silica exposure, serum and bronchoalveolar lavage fluid (BALF) samples were obtained. The concentration of SP-A, SP-B, SP-C, SP-D in serum and BALF were measured by using enzyme immunoassay (ELISA). Meanwhile the levels of total anti-oxidative activity (T-AOC) and hydroxyproline (HYP) in lung tissue were also detected. The pathology of lung tissue was conducted.

RESULTSCompared with control group, SP-A concentration in BALF of silica exposed rat for 3, 14, 21, 28d was significant lower and SP-D concentration in BALF of silica exposed rat for all time points was also lower. The differences were significant (P < 0.05). Meanwhile SP-B level in 7, 14, 21, 28 d silica exposed rats BALF and SP-C level in 14, 21, 28 d silica exposed rats markedly decreased (P < 0.05). In addition compared with control group, SP-A, SP-B and SP-C concentration in serum of silica exposed rat were higher when SP-A for 14, 21, 28 d silica exposure, SP-B for 7, 14, 21 d silica exposure and Sp-C for 7, 14, 21, 28 d exposure. And all difference were significant (P < 0.05). As silica exposure time increased, SP-C concentration in serum showed an increase trend, which showed a time-response relationship (r = 0.618, P = 0.042). However, SP-D concentration in serum of rat for 7, 14, 21, 28d silica exposure were significant lower than that of control group (P < 0.005). And there was a decrease trend with time point exposure regarding of SP-D (r = -0.731, P = 0.016). The HYP content in lung tissue of experiment rats increased at 3rd, 7th, 14th, 21st and 28th day time point and The T-AOC activity in lung tissue decrease at, 7th, 14th, 21st and 28th day time point. The differences were significant (P < 0.05). There was a positive correlation (P = 0.803, P = 0.045) between SP-C in BALF and HYP of silica exposed rats and a negative correlation between SP-D in BALF and HYP (r = -0.867, P = 0.033). No significant correlation were seen between SP-A, SP-B BALF and HYP (y = 0.416, P = 0.28; r = 0.592, P = 0.071). SP-C concentration in BALF and serum all showed an increased trend and a positive correlation was seen (r = 0.539, P = 0.046). The same decrease trend was seen between SP-D in BALF and serum and correlation value was 0.870 (P = 0.034).

CONCLUSIONThe silica exposure did cause the change of SP content both in BALF and serum. The SP-C and SP-D content in serum might be served as an early effective biomarker of silicosis.

Animals ; Bronchoalveolar Lavage Fluid ; Male ; Pulmonary Fibrosis ; metabolism ; pathology ; Pulmonary Surfactant-Associated Proteins ; metabolism ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide ; Silicosis ; metabolism ; pathology

BACKGROUND: All organisms have developed an internal timing system capable of reacting to and anticipating environmental stimuli with a program of appropriately timed metabolic, physiologic and behavioral events. The alveolar epithelial type II cell of the mammalian lung synthesizes, stores, and secretes a lipoprotein pulmonary surfactant, which functions to stabilize alveoli at low lung volumes. METHODS: The authors investigated the diurnal variation of surfactant protein A, B and C mRNA accumulation. The diurnal variation on gene expression of surfactant protein A, B and C was analysed using filter hybridization at 9 a.m., 4 p.m. and 11 p.m. Lung SP-A protein content was determined by double sandwich ELISA assay using a polyclonal antiserum raised in rabbits against purified rat SP-A. RESULTS: 1. The accumulation of SP-A mRNA at 4 p.m. was significantly decreased by 23.5% compared to the value at 9 a.m. (p< 0.05). 2. The accumulation of SP-B mRNA at 4 p.m. and 11 p.m. was decreased by 15.1% and 5.7%, respectively, compared to the value at 9 a.m. (p=0.07, p=0.69). 3. The accumulation of SP-C mRNA at 4 p.m. and 11 p.m. was decreased by 6.8% and 7.7%, respectively, compared to the value at 9 a.m. (p=0.38, p=0.57). 4. Total lung SP-A content at 4 p.m. and 11 p.m. was increased by 5.3% and 15.9%, respectively, compared to the value at 9 a.m. (p=0.64, p=0.47). CONCLUSION: These findings represent the diurnal variation of surfactant proteins mRNA expression in vivo. These results indicated that the diurnal variation of significant gene expression is observed in hydrophilic surfactant protein rather than in hydrophobic surfactant proteins.
Animals ; *Circadian Rhythm ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; Pulmonary Surfactant-Associated Proteins/genetics/*metabolism ; RNA, Messenger/*metabolism ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the effects of ischemic preconditioning on reperfusion injury of rat lung.

METHODSRat isolated lungs (n=8 in each group) were stabilized and perfused by Krebs-Henseleit solution on a modified langendorff perfusion apparatus. 36 wistar rats were divided into three groups: ischemic preconditioning group, ischemia/reperfusion group and control group. Mean pulmonary artery pressure, wet/dry ratio, pulmonary surfactant phospholipid and alveolar surface tension in bronchoalveolar lavage fluid and electron microscope were detected.

RESULTSThe morphological changes of lung injury were alleviated in the preconditioning group under electron microscope. Wet/dry ratio, mean pulmonary artery pressure and SA/LA ratio were significantly lower in the preconditioning group after ischemic/reperfusion (P < 0.01). Total phospholipid and large aggregate in the BALF were significantly increased in the preconditioning group (P < 0.01). Small aggregate showed no change in three groups. Surfactant activity test showed that surface tension markedly decreased in IPC group (P < 0.01).

CONCLUSIONThese results indicates that ischemic preconditioning may have a protective effect in ischemic/reperfusion injuries lung by ameliorating the content and function of surfactant phospholipid.

Animals ; Ischemic Preconditioning ; methods ; Lung ; blood supply ; metabolism ; pathology ; Pulmonary Surfactant-Associated Proteins ; secretion ; Rats ; Rats, Wistar ; Reperfusion Injury ; prevention & control