支气管肺发育不良患儿肺表面活性蛋白-B内含子4基因多态性

目的 了解支气管肺发育不良( bronchopulmonary dysplasia,BPD)患儿肺表面活性蛋白-B(surfactant protein-B,SP-B)内含子4基因多态性的改变. 方法 对2008年7月至2011年7月在华中科技大学同济医学院附属同济医院新生儿重症监护病房收治的45例BPD患儿(BPD组)采用聚合酶链反应技术、琼脂糖凝胶电泳分离以及克隆测序法行SP-B内含子4片段长度多态性检测,并以无肺部疾病的99例患儿为对照(对照组),分析其等位基因[野生等位基因、变异等位基因(插入等位基因和缺失等位基因)]频率和基因型[野生型、变异型(插入型和缺失型)]频率在2组间的差异.研究结果采用两样本均数t检验或x2检验进行统计学分析. 结果 BPD组与对照组野生等位基因频率分别为83.3％(75/90)和91.9％ (182/198),变异等位基因频率分别为16.7％(15/90,其中插入等位基因8例,缺失等位基因7例)和8.1％(16/198,其中插入等位基因8例,缺失等位基因8例),2组比较差异有统计学意义(x2 =4.75,P=0.029).BPD组基因型频率野生型为71.1％(32例),变异型为28.9％(13例,其中插入型7例,缺失型6例),对照组野生型为85.8％(85例),变异型为14.1％(共14例,插入型6例,缺失型8例),2组比较,差异有统计学意义(x2=4.42,P=0.036). 结论 BPD患儿SP-B内含子4基因变异发生率高,提示SP-B内含子4变异可能与BPD遗传易感性相关.     

支气管肺发育不良患儿早期应用肺表面活性物质的临床价值分析

目的分析支气管发育不良(BPD)患儿早期应用肺表面活性物质(PS)的临床价值。方法 2013年3月至2016年5月河南宏力医院新生儿科收治住院的BPD患儿68例,随机分为观察组和对照组各34例。对照组予以常规机械通气、吸氧治疗,观察组加用PS治疗。比较两组吸氧时间、机械通气时间及肺功能。两组均持续治疗2周。结果观察组吸氧时间与机械通气时间较对照组均明显缩短,差异有统计学意义(P0.05);观察组1岁、2岁时肺功能明显优于对照组,差异有统计学意义(P0.05)。结论早期应用PS治疗BPD效果显著,可明显缩短机械通气时间,减轻肺损伤,改善肺功能,值得推广。     

布地奈德联合肺表面活性物质对早产儿支气管肺发育不良的临床疗效

目的 探讨布地奈德联合肺表面活性物质(PS)预防早产儿支气管肺发育不良(BPD)的发生.方法 选取2018年1月至2020年6月本院收治的呼吸窘迫综合征早产儿80例为研究对象,随机分为对照组和观察组各40例.对照组给予PS治疗,观察组给予布地奈德联合PS治疗.分析两组患儿治疗期间主要并发症、BPD发生率及严重程度、持续...     

肺表面活性物质替代治疗对支气管肺发育不良发病的影响

目的　探讨肺表面活性物质 (PS)替代治疗对支气管肺发育不良 (BPD)发生率的影响。　方法　采用单剂 Exosurf气管内治疗 2 5例新生儿呼吸窘迫综合症 (NRDS)患儿 ,并与同期未用 PS治疗的 2 5例 NRDS患儿进行前瞻性非随机对照研究 ,统计 BPD的发生情况。　结果　 PS运用组机械通气及氧疗时间较未用 PS组明显缩短 ,机械通气的天数由 (13± 9) d下降为 (6± 4) d,氧疗天数由(2 1± 9) d下降为 (9± 6 ) d,差异有显著性意义。BPD的发生率由 40 %下降至 2 0 % ,差异无显著性意义。　结论　 PS治疗 NRDS患儿能缩短机械通气的时间及氧疗天数 ,但是否减少 BPD的发生率 ,尚需进一步操讨     

新生儿支气管肺发育不良死亡1例

目的：通过此病例探讨新生儿出生后死亡的原因。方法：通过对病例中产妇产程分析,新生儿出生后Apgar氏评分情况分析,结合胸部X正位片表现,探讨新生儿死亡原因。结果：摄胸平提示：胸片提示双侧胸廓对称,新生儿双侧胸腔未见肺纹理,无明显肺泡结构,心膈显示不清,心膈,纵膈及双侧顶正常结构消失,多考虑先天性支气管肺发育不良（BPD）。结论：新生儿死亡原因为支气管肺发育不良（BPD）。     

肺表面活性物质相关蛋白、血清铁蛋白及肿瘤坏死因子α与新生儿呼吸机相关性肺损伤发病的关系

随着新生儿急救技术的不断进步和完善，机械通气在NICU中的使用频率越来越高，同时又不可避免出现各种不同并发症，如呼吸机相关性肺损伤（ventilator associated lung injury，VALI）、支气管肺发育不良（bronchopulmonary dysplasia，BPD）、呼吸机相关性肺炎等，影响患儿日后生存质量。其中呼吸机相关性肺损伤是机械通气治疗过程中出现的严重并发症之一。现就肺表面活性物质相关蛋白（surfactant-associated protein，SP）、     

新生儿肺部疾病支气管肺泡灌洗液肺表面活性蛋白A的检测及意义

目的 探讨新生儿常见肺部疾病支气管肺泡灌洗液肺表面活性蛋白A(BAL SP-A)水平及其与临床的关系。方法 收集2000年1月至2003年2月在广州市儿童医院新生儿重症监护室住院的需行机械通气治疗的新生儿重症肺炎、胎粪吸入综合征(MAS)、急性呼吸窘迫综合征(ARDS)以及新生儿呼吸窘迫综合征(RDS)患儿共57例。测定其BAL SP-A水平，监测血气、PaO2/FiO2水平。结果重症肺炎组与MAS组患儿BAL SP-A水平无明显差异，但MAS组患儿PaO2、PaCO2及PaO2/FiO2水平较重症肺炎组明显降低(P值<0.01,<0.05,<0.05)；ARDS及RDS组患儿BAL SP-A水平均较上述两组低(P值均<0.001)，而RDS组患儿BAL SP-A水平较ARDS组低(P<0.001)，但ARDS组患儿PaO2水平较RDS组患儿低(P<0.05)。PS治疗组患儿的病死率较非PS治疗组明显降低(P=0.049)，其PaO2/FiO2与BAL SP-A水平密切相关(r=0.741,P=0.000)。结论 与重症肺炎患儿比较胎粪吸入综合征患儿BAL SP-A水平无明显降低；ARDS及RDS患儿BAL SP-A水平明显降低；BAL SP-A水平能反映新生儿肺损伤的严重程度，对于新生儿肺部疾病预后的判断有一定意义。 Abstract ObjectiveTo investigate the bronchoalveolar lavage (BAL) SP-A concentrations from newborn infants with lung disease,and to study the relationship between BAL SP-A and clinical outcome.Methods 57 cases of newborn infants with lung disease were admitted in our NICU between Jan.2000 and Feb.2003.BAL SP-A concentrations,PO2 value,PCO2 value,and PaO2/FiO2 ratio were measured.ResultsBAL SP-A concentrations did not differ between severe pneumonia group and MAS group,but the value of PaO2、PaCO2 and PaO2/FiO2 ratio in MAS group were significantly lower than that in severe pneumonia group (p respectively<0.001,<0.05,<0.05).BAL SP-A concentrations in RDS and ARDS groups were significantly lower than that in aforesaid groups ( all P<0.05).BAL SP-A concentrations in RDS group were significantly lower than that in ARDS group,but PaO2 value in ARDS group was lower significantly than that in RDS group( P<0.05).The mortality of infants treated with PS was significantly lower than that of infants treated without PS (P=0.049).PaO2/FiO2 ratio for the cohort was related to their BAL SP A concentrations ( r=0.741,P=0.000).Conclusion Surfactant protein A content in MAS is not different from that of severe pneumonia.BAL SP-A concentrations of neonates with ARDS or RDS decrease significantly.BAL SP-A concentrations can evaluate the severity of lung injury and the prognosis of neonatal lung disease. Key wordsInfant,newbornLung disease;Bronchoalveolar lavae;Surfactant protein A     

早产儿支气管肺发育不良症的早期诊断和治疗

目的　探讨早产儿支气管肺发育不良症 (BPD)的早期诊断和治疗。　方法　对 1994年 1月～ 1999年 1月在我院 NICU住院的 12例 BPD患儿的发病、临床诊断和应用地塞米松治疗进行观察和总结 ,并对所有患儿在出院后 6～ 12个月内进行了随访。　结果　经用地塞米松治疗 ,12例患儿全部治愈出院 ,住院时间 31～ 6 7(5 0± 14) d。随访 1年 ,11例预后良好 ,1例仍反复呼吸道感染。BPD是患呼吸窘迫综合征 (RDS)的极低出生体重儿应用机械通气治疗后的常见合并症。患 RDS的早产儿中 ,发生 BPD者 ,其胎龄及出生体重明显低于未发生 BPD者 (P<0 .0 0 1) ;而其机械通气的最高吸气峰压和吸入氧浓度亦明显高于未发生 BPD者 (P<0 .0 1)。　结论　对易感儿在治疗过程中应严密观察临床征象和辅助检查 ,尽早做出诊断 ,及时应用地塞米松治疗可取得较好的效果。     

缺氧诱导丝裂原因子对胎肺形态发育及表面活性蛋白表达的影响

目的 探讨缺氧诱导丝裂原因子(hypoxia-induced mitogenic factor,HIMF)对胎肺形态发育及表面活性蛋白B(surfactant protein B,SP-B)、表面活性蛋白C(snrfactant protein C,SP-C)表达的调控作用.方法 体外分离、培养小鼠第13.5天胎肺组织,分为HIMF处理组:在培养基中添加重组HIMF蛋白,终浓度为100 nmol/L;对照组培养基中不加任何处理.分别在培养0、48、72 h后,每组每时间点选取20例胎肺采用倒置显微镜和HE染色观察胎肺形态学和组织学的改变,采用Western印迹、免疫组化、实时逆转录-聚合酶链反应技术检测胎肺组织中SP-B和SP-C的蛋白、mRNA表达水平变化.结果 HIMF处理组培养48、72 h后,肺泡数目分别为(14.37±0.85)和(18.41±1.24)个/高倍视野,肺泡分支的数目分别为(2.51±0.35)和(3.28±0.51)个/高倍视野,均较对照组相应时间点[分别为(8.09±0.92)、(9.54±0.78)、(1.45±0.32)和(1.69±O.43)个/高倍视野]增加,差异有统计学意义(P<0.05).对照组胎肺体外培养72 h后,SP-B、SP-C蛋白表达较少,染色强度弱,主要定位于Ⅱ肺泡上皮细胞;HIMF处理组可见Ⅱ型肺泡上皮细胞内SP-B、SP-C弥漫表达,以靠近肺组织边缘为甚.HIMF处理组培养48和72 h后,胎肺组织中SP-B、SP-C蛋白和mRNA水平均较对照组相应时间点增加,差异有统计学意义(P<0.05).结论 HIMF可能通过上调胚胎组织中SP-B和SP-C的表达,促进胎肺形态发育,为进一步研究HIMF在胚胎肺泡发育和成熟中的作用奠定了基础.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

目的 探讨肺透明膜病(HMD)早产儿经机械通气/高氧或肺表面活性物质(PS)替代治疗后其尸检肺组织肺表面活性蛋白-C(SP-C)及增殖抗原Ki67表达情况,分析临床治疗与病理改变的关系.方法 临床和病理确诊为HMD的早产儿,因HMD而在生后6 h内接受机械通气及高浓度氧(FiO20.6～1.0)治疗无效死亡者30例.按接受机械通气/高氧治疗时间的长短,分1～3 d、4～8 d、9～16 d和>16 d共4组,其中13例患儿同时接受了PS治疗.以无肺部疾病的5例早产儿为对照.应用免疫组织化学方法检测尸检肺组织标本中SP-C及Ki67的表达.多组间比较采用方差分析及g检验.结果 机械通气/高氧治疗的HMD早产儿,其不同时期肺组织的病理表现符合HMD向支气管肺发育不良转变的病理特征.肺组织SP-C表达定位于Ⅱ型肺泡上皮细胞,Ki67表达主要定位于肺、支气管上皮细胞和肺成纤维细胞.机械通气/高氧治疗1～3 d,SP-C及Ki67表达的平均光度值分别为0.1576±0.0327和0.1929±0.0403,较对照组(0.1891±0.0253、0.2297±0.0380)明显降低(P均<0.05);4 d后,SP-C及Ki67表达均逐渐升高,至9～16 d左右达高峰,分别为(0.2410±0.0225、0.2987±0.0116).PS治疗组与无PS治疗组肺组织SP-C及Ki67表达差异无统计学意义(t值分别为2.007和0.458,P均>0.05).结论 SP-C及Ki67表达改变参与了HMD早产儿机械通气/高氧治疗后肺组织的病理发展过程;PS治疗对SP-C及Ki67表达无明显影响.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.     

肺透明膜病早产儿尸检肺组织肺表面活性蛋白-C及Ki67的表达

Objective To determine the expression of surfactant protein-c (SP-C) and Ki67 in autopsy lung tissues of premature infants died of hyaline membrane disease (HMD) who were exposed to mechanical ventilation and high oxygen concentrations/pulmonary surfactant (PS). The possible influence of surfactant on the expression of SP-C and Ki67 was also investigated. Methods Thirty preterm infants diagnosed as HMD by clinical data and pathology were selected. Mechanical ventilation and supplemental oxygen (FiO2 0.6-1.0) were given to these infants within 6 hours after birth. According to the duration of ventilation at high oxygen concentrations, all subjects were diveded into four groups: ventilation for 1-3 days, 4-8 days, 9-16 days and >16 days. Five premature infants died within 1 day after delivery for none pulmonary reasons served as controls. The expression of SP-C and Ki67 in lungs were detected by immunobistochemistry. Results The pulmonary pathology in these HMD infants at different phases was consisitent with the main features of different stages during the progress from HMD towards bronchopulmonary dysplasia. The positive staining of SP-C was restricted to type Ⅱ alveolar epithelial cells, and Ki67 positive were preferentially localized in nuclei of alveolar and bronchiolar epithelial cells and fihroblasts. Compared with the control group, the expression of SP-C and Ki67 in HMD infants decreased significantly after 1-3 days of ventialation, but increased after 4 days and reached the peak value after 9-16 days. The expression of SP-C and Ki67 in control group, 1-3 days and 9-16 days of ventialation were 0. 1891±0. 0253, 0. 1576±0. 0327 and 0. 2271±0. 0238 for SP-C and 0. 2297±0. 0380, 0.1929±0. 0403 and 0. 2849±0. 0368 for Ki67, respectively. No significant difference in the expression of SP-C and Ki67 was found between infants treated with PS and those without (P>0.05). Conclusions SP-C and Ki67 may have participated in the pulmonary pathological process in ventilated/oxygen treated preterm infants with HMD, and exogenous surfactant had no effect on the expression of SP-C and Ki67.