Bronchopulmonary dysplasia (BPD) is a respiratory disorder that is frequently associated with premature infants.Prevention from its occurrence is perceived to be more valuable than its treatment due to the current lack of effective management.This article elaborated recent development in preventing premature birth and lung injuries caused by mechanical ventilation,oxygen toxicity,infection and inflammation,which played a central role in the development of BPD.

Bronchopulmonary dysplasia ( BPD) ,also called chronic lung disease ( CLD) ,is a com-mon respiratory disease of premature infants. It was first reported and named by Northway et al, carrying unique etiology,pathology and clinical features. BPD reported by Northway is referred as old or classic BPD. Manifestations and prognosis of premature infants with respiratory diseases have been improved significantly after evolutional changes by applying glucocorticoid and exogenous surfactant,as well as protective ventilator protocols after birth. Nowadays,incidents of severe BPD described by Northway are extremely low,whereas mild BPD,also called ‘new’ BPD,is much more common. Definition and nomenclature of BPD have been controversial since first being brought out in 1967. This article was focused on the definition and nomenclature and current advances in BPD treatment.

The fetal inlfammatory response syndrome (FIRS) is a subclinical condition characterized by systemic acti-vation of the fetal innate immune system with a large number of pro-inlfammatory cytokines released. FIRS is the fetal coun-terpart of the systemic inlfammatory response syndrome (SIRS) described in adults. Intrauterine infection is the most common reason of FIRS. FIRS has been implicated as a cause of preterm labor, preterm white matter injury, bronchopulmonary dyspla-sia (BPD) and necrotizing enterocolitis (NEC).

A method for determinattion of monoamine neurotransmitters and related compounds in microdialysis solution by high performance liquid chromatography (HPLC) with pulsed amperometric detection was described. A comparison of response of iso potential anperometric (AD) and pulsed amperometric detection (PAD) was made. The results indicated that the sensitivity of PAD was 1.2 fold that of AD. The quantitative determination of monoamine neurotransmitters and related compounds was carried out with 3,4-dihydroxybenzylamine (DHBA) as internal standerd. The recoveries of monoamine neurotransmitters in microdialysis solution are 71% ～ 101%.

Objective To explore effect of hyperoxia and amygdalin on surfactant associated protein messenger RNA levels of alveolar epithelial cells of premature rat lung. Methods Type Ⅱ alveolar epithelial cells (AECⅡ) were gained by primary culture from 19-days fetal rat lung. After purified,AECⅡ were randomly assigned to four groups and exposed to air or hyperoxia: air group (group Ⅰ),hyperoxia group (group Ⅱ),air plus amygdalin group (group Ⅲ),hyperoxia plus amygdalin group (group Ⅳ),Groups Ⅱ、Ⅳ were flushed the flake with 95% oxygen-5% CO 2 at 3 L/min for 10 min,then sealed and cultured for 24 hours. Groups Ⅲ,Ⅳ were added 200 ?mol/L of amygdalin at the same time. All groups were in CO 2 culture chamber (37 ℃,5% CO 2) for 24 hours,cells were harvested and extracted for total RNA by Trizol reagent. mRNA levels of SP were measured by reverse transcription polymerase chain reaction (RT-PCR). Results SP mRNA levels were significantly decreased in groupⅡ compared to groupⅠ( P

Objective To explore the influence of retinoic acid (RA) on the expressions of insulin-like growth factor (IGF)-Ⅱ,type 2 IGF receptor (IGF-2R) and IGF binding protein (IGFBP)-2 mRNA and polypeptides in lungs of hyperoxia-exposed premature rats and its possible molecular mechanism. Methods On the 2nd postnatal day, 260 Sprague-Dawley(SD)preterm rats were randomly divided into 4 groups. Group Ⅰ: air + normal saline (NS) group; Group Ⅱ: hyperoxia(85% O_2) + NS group; Group Ⅲ: air+ RA group; Group Ⅳ: hyperoxia(85% O_2) + RA group. RA was injected to group Ⅲ, Ⅳ intraperitoneally (500 ?g/kg) since the 3rd day after birth, while NS was given to group Ⅰ,Ⅱ daily at the same time as group Ⅲ and Ⅳ. On day 4, 7, 10, 14 and 21 after birth, 8 rats in each group were killed. The mortality of preterm rats was recorded and lung radical alveolar counts (RAC) were examined. The mRNA analysis (RT-PCR) and polypeptides analysis (Western Blot) of IGF-Ⅱ, IGF-2R and IGFBP-2 were performed. Results 1. On the 4～7th day of exposure, the survival rate in all groups were similar. After 7 days of 85% O_2 exposure, the survival rate in group Ⅱ, Ⅳ dropped sharply and there was a significant difference comparing to group Ⅰ, Ⅲ( P

Objective To study the risk factors for failure of INSURE strategy in very and extremely low birth weight preterm (V/ELBW) infants.Method From January 2005 to December 2014,clinical data of 149 preterm infants (gestational age less than 32 weeks) admitted to neonatal department of Tongji Hospital who received intubation-surfactant-extubation (INSURE) strategy were collected.These infants were assigned into two groups:INSURE failure group and INSURE success group,according to whether a second dose of surfactant or mechanical ventilation was needed within 72 hours after first pulmonary surfactant treatment.The clinical characteristics and outcomes between the two groups were compared.Chi square and t tests were used to define the differences between groups.Logistic regression analysis was used to identify the independent risk factors for INSURE failure.Result Among the 1 149 patients,148 received INSURE treatment,and 113 cases (76.4％) were successfully treated with the INSURE strategy.The infants in the failure group were statistically lower in birth weight,gestation age,antenatal steroids utilization rate,PaO2 and PaO2/FiO2 than those in the success group,while the age of mother,male/female ratio and PaCO2 were higher in the failure group.Logistic regression analysis showed that male (OR =7.440,95％ CI 1.846 ～29.984),BW ＜ 1 000 g (OR =9.180,95％ CI 1.716 ～49.105),PaCO2 ＞48 mmHg (OR =5.996,95％ CI 2.088 ～ 17.213),PaO2/FiO2 ＜205 (OR =3.010,95％ CI 1.033 ～8.774) were independent risk factors for INSURE failure.Conclusion INSURE strategy failure was associated with gender,birth weight,gestation age,antenatal steroids utilization,PaO2,PaCO2 and PaO2/FiO2 of the first blood gas after birth.BW ＜ 1 000 g,PaCO2 ＞ 48 mmHg and PaO2/FiO2 ＜ 205 of the first blood gas after birth were independent risk factors for INSURE strategy failure.

Objective To investigate the therapeutic mechanism of dexamethasone in hyperoxia-induced lung injury. Methods Use bronchoalveolar lavage (BAL) method to gain alveolar macrophages (AM) from newborn SD rats. AM were adherence purified for 24 hours, then randomly assigned to four groups: Ⅰ. hyperoxia group, Ⅱ. hyperoxia plus LPS group, Ⅲ. hyperoxia plus dexamethasone group, Ⅳ. hyperoxia plus LPS plus dexamethasone group. Every group contains 7 samples. After cultured for 48 hours, supernatants were harvested. L-lactate dehydrogenase (LDH) activity? hydrogen peroxide (H 2O 2) and IL-8 contents of supernatants were examined in all groups. Results (1)48 h after culture, the content of IL-8 in groupⅠandⅡwas (46?15)pg/ml?(145?27)pg/ml respectively, in groupⅢandⅣwas(29?4)pg/ml?(39?8)pg/ml respectively, IL-8 content was decreased in group Ⅲ and Ⅳcompared with group Ⅰand Ⅱ(P

Objective To explore the role of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in hyperoxia-induced lung injury in preterm rats. Methods At the 2 nd postnatal day Sprague-Dawley preterm rats were randomly assigned to air group and hyperoxia group (exposed to about 85% of O 2). At 3,7,14 and 21 days after exposure, six rats of each group were used to assess lung histologic changes and expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 in lungs by immunohistochemistry. At 3,7 and 14 days after exposure, gelatinase activity in bronchoalveolar lavage fluid (BALF) of another six rats in each group by gelatin zymography was examed. Results Except 3 d after exposure, hyperoxia group showed lung injury characterized by subacute alveolitis and inhibition of lung development. Expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 in hyperoxia group was stronger than that in air group at every time (P

To explore the mechanism of Notch in hyperoxia-induced preterm rat lung injury, 2-days-old preterm SD rats were randomized into control and hyperoxia group (FiO2 > or = 0.85). On day 1, 7, 14 and 21, 8 rat pups of each time point were used to assess histopathological changes of lung with HE staining and to evaluate the expression of Notch1 and Notch3 with immunohistochemistry. Notch1, Notch3, Aquaprin5 (AQP5) and surfactant protein C (SP-C) mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). The results showed that the lung injury in the hyperoxia group was characterized by retarded lung alveolization and differentiation of alveolar epithelial type II cells (AEC II). Positive staining of Notch1 in hyperoxia group was weaker than controls at every time point (except for day 7), while positive staining of Notch3 was much stronger (P < 0.05, P < 0.01). Notch1, Notch3 mRNA level showed similar change as protein level. AQP5, SP-C mRNA decreased significantly as compared with that of the controls (P < 0.01). We are led to conclude that hyperoxia results in abnormal expression of Notch, which is likely to contribute to the pathogenesis of lung injury through regulating proliferation and transdifferentiation of alveolar epithelial cells.
Aerobiosis ; Animals, Newborn ; Lung/*pathology ; Lung Diseases/etiology ; Lung Diseases/*metabolism ; Lung Diseases/pathology ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Random Allocation ; Rats, Sprague-Dawley ; Receptors, Notch/*biosynthesis ; Receptors, Notch/genetics