首剂大剂量肺表面活性物质治疗重度新生儿肺透明膜病临床观察

目的比较首剂不同剂量的肺表面活性物质(PS)对新生儿肺透明膜病(HMD)治疗效果的影响。方法随机将2006年6月至2007年6月广东省妇幼保健院48例Ⅲ、Ⅳ级HMD早产儿分为两组：首剂大剂量组(PS治疗剂量150~200 mg/kg)和首剂小剂量组(PS治疗剂量50~100 mg/kg)。比较两组患儿用药次数、用药总剂量,使用6 h后血气分析,PaO2/FiO2,呼吸机通气治疗时间以及监护室住院时间等。结果两组治疗用药总剂量差异无统计学意义,首剂大剂量组的机械通气时间、氧疗时间、监护室住院时间显著低于首剂小剂量组,治疗后6 h两组的PaO2,PaO2/FiO2均显著升高,但升高程度两组间差异无统计学意义。结论PS首剂治疗量达150~200 mg/kg时治疗重度HMD的效果优于首剂治疗量为50~100 mg/kg,值得在临床中推广。     

肺表面活性物质的运用与新生儿肺透明膜病的转归

目的　探讨肺表面活性物质（Ｅｘｏｓｕｒｆ） 治疗新生儿肺透明膜病（ＨＭＤ） 的疗效及其并发症。　方法　采用回顾性分析的方法对用药前、用药后３０ 分钟及用药后６ 小时血气指标,机械通气参数进行比较分析,通过肺氧合情况判断疗效,分析转归及并发症。　结果　１６ 例患儿血气指标及机械通气的参数用药前与用药后６ 小时比较差异有显著性,氧分压（ＰＯ２） 由（４１－６ ±６ ．０）ｍ ｍ Ｈｇ（１ｍ ｍ Ｈｇ＝０ ．１３ ｋＰａ） 升高至（６２－９ ±２－０） ｍ ｍ Ｈｇ,动脉压泡氧分压比值（ａ／ＡＰＯ２） 由（０－１２ ±０－０３）ｍ ｍＨｇ 升高至（０－２４ ±０－１１）ｍ ｍ Ｈｇ,ＰＯ２／ＦｉＯ２ 由（７４－６ ±１６－４）ｍ ｍＨｇ 升高至（１４７－４ ±５９－９）ｍ ｍＨｇ,ＦｉＯ２ 由０－５８±０ ．０７ 降至０－４５ ±０ ．０９ ,ＭＡＰ由（１３－０ ±１．３）ｍ ｍ Ｈｇ 降至（１１－１ ±１－６）ｍｍ Ｈｇ。２４ 小时内复查胸片１３ 例明显好转,２ 例无改变,１ 例合并肺出血。其中痊愈１２ 例（治愈率７５ ％ ）,死亡２ 例,放弃２ 例。　结论　肺表面活性物质（Ｅｘｏｓｕｒｆ） 的运用可以改善肺透明膜病的转归,降低病死率     

新生儿甲状腺功能减低症并肺透明膜病一例

新生儿甲状腺功能减低症简称甲低又称克汀病或呆小症,甲低是由于甲状腺激素的合成及分泌不足或靶细胞受体缺陷,引起的代谢水平低下、体格和智能发育障碍。国内发病率为1/7000,而甲低并肺透明膜病较罕见。我院经治的一例报告如下。患儿女2小时,因生后气促、发绀1小时入院。患儿系第1胎第1产,母孕期顺利,否认遗传和家族病史。孕39~((?)6)周剖腹产分娩,Apgar     

高频振荡通气治疗重症新生儿肺透明膜病疗效观察

目的：探讨高频振荡通气（HFOV）治疗重症新生儿肺透明膜病（HMD）的疗效及其安全性。方法：10例重症新生儿肺透明膜病常频机械通气条件达到PIP24cmH2O,PEEP4-6 cmH2O,MAP≥13 cmH2O,FiO2≥0.6,PaO2〈50mmHg或PaCO2＞65mmHg。改换高频振荡通气,观察治疗前后血气指标的变化及临床疗效。结果： HFOV治疗后PaCO2、氧合指数（0I）和FiO2稳步降低,PaO2和TcSO2稳步升高（均P〈0.05）,10例全部治愈,无1例发生气漏,9例存活早期早产儿3例轻度慢性肺疾病（CLD）发生,发生颅内出血2例,均为室管膜下-脑室内出血Ⅰ-Ⅱ级。结论：高频振荡通气治疗HMD,是一种疗效肯定、安全性好的新型机械通气方法。     

盐酸氨溴索与激素联合使用预防新生儿肺透明膜病

目的研究在应用肾上腺糖皮质激素的基础上加用盐酸氨溴索(沭舒坦)预防新生儿肺透明膜病的效果.方法将1999年1月至2001年6月我院出生的早产儿分为3组实验1组激素加产前用沐舒坦组;实验2组激素加产前或产后用沭舒坦组;对照组;单用激素组.比较3组新生儿肺透明膜病(HMD)的发生率.结果实验1组、2组HMD的发病率均为0%,对照组为16.67%,高于两组实验组,统计学差异有显著意义(P＜0.05).结论①产前在使用激素的基础上加用沭舒坦可预防HMD的发生,疗效优于单用激素预防.②从总体而言,在母亲产前使用激素的基础上,不论是采用产前孕母加用沐舒坦,还是产后新生儿用沐舒坦,均可有效降低HMD的发生率,疗效优于单用激素预防.     

早产儿肺透明膜病的临床X线分析

目的：分析早产儿肺透明膜病的x线特征及早期x线表现,提高对本病的认识和早期诊断、旱治疗。方法：回顾2010至2（112年间在我院生产的早产儿肺透明膜病56例的临床资料不同时龄x线仰卧位吸气胸片。结果：轻度（I、Ⅱ级）47例,其中12例中下野两肺纹理边缘模糊,表现小网格样及小颗粒状增高影,肺野透亮度减低,32例有心影后支气管充气征中度（3级）7例,表现两肺野呈细磨玻璃样和粗磨玻璃样改变,均有明显支气管充气征。心缘较模糊和毛糙;重度（Ⅳ级）双肺野透明度极低（白肺）,未见支气管充气征,心缘及膈面消失,肋膈角可见。本组病例中一例伴有间质性肺水肿,一例纵膈积气,见胸腺抬高征。结论：早产儿肺透明膜病x线仰卧位吸气胸片是简捷、实用的检查方法。两下肺纹理边缘模糊。内中带小网格及小颗粒状增高影、透亮度减低、心影后支气管气征是HMD的早期x线表现。     

乐舒凡预防早产儿肺透明膜病的临床研究

目的：评价乐舒凡预防新生儿肺透明膜病的临床疗效。方法将73例胎龄29W～35W、体重1200g～2250g的早产儿随机分为两组,预防组生后2小时内口服或胃管注入乐舒凡,对照组不用乐舒凡,两组患儿均给予相同的综合治疗,比较两组患儿发生肺透明膜病的机率、及发生肺透明膜病后需要转院治疗的例数。结果预防组肺透明膜病发生率及发生肺透明膜病后需要转院治疗的例数均比对照组少,二者比较有统计学意义（P〈0.05）。结论在基层医院早产儿生后早期应用乐舒凡,对减少NRDS的发生及减轻NRDS的严重程度是有效的。     

新生儿肺透明膜病附43例床边胸片随访分析

目的：探讨新生儿肺透明膜病的影像学特征及床边胸片随访复查的意义。方法：回顾性分析43例经床边胸片随访复查及临床证实的新生儿肺透明膜病。结果：15例为I级,8例为ii级,10例为Ⅲ级,10为Ⅳ,并发肺部感染5例,气胸4例（其中1例合并气腹）。结论：新生儿肺透明膜病有典型的特征性x线表现,床边胸片随访对本病病情变化,并发症的发现及临床治疗疗效具有重要的价值。     

盐酸氨溴索早期防治新生儿肺透明膜病疗效观察

目的观察盐酸氨溴索早期防治新生儿肺透明膜病（HMD）的效果。方法将104例早产儿按随机数字表法分为两组,观察组53例,对照组51例。对照组进行常规综合治疗,观察组在常规治疗基础上加用盐酸氨溴索30mg/（kg.d）,分4次加入5%葡萄糖溶液5mL稀释后微量泵入,每次泵入10min,疗程3d。观察两组患儿治疗后的临床表现,经皮血氧饱和度及胸片,比较两组早产儿HMD的发生率。结果观察组HMD发生率为7.5%（4/53）,低于对照组27.5%（14/51）,差异有统计学意义（χ2=7.19,P〈0.05）;观察组患儿无一例死亡,对照组死亡6例。结论盐酸氨溴索对预防HMD的发生有较好疗效,能改善通气,降低死亡率,早期应用可降低HMD的发生率;在发生HMD后可减少气管插管,减少机械通气率,疗效确切,经济安全。     

44例围产儿肺透明膜病的临床和病理研究

目的探讨围产儿肺透明膜病的临床意义、发病机理及其与缺氧缺血性脑病的关系。方法在分析常规;临床和病理资料的基础上,用尸肺灌洗液进行表面活性物质测定。结果病理检查显示肺组织广泛不张及透明膜形成,肺泡Ⅱ型上皮细胞受损及呼吸膜断裂。88％的患儿继发缺血性脑病。结论肺发育不成熟,肺泡Ⅱ型上皮细胞受损,肺表面活性物质缺乏,呼吸膜断裂是本病的主要原因。     

The association between hyaline membrane disease and preeclampsia

OBJECTIVE: The purpose of this study was to determine whether hyaline membrane disease is increased in newborn infants who are born to women with preeclampsia compared with control subjects. STUDY DESIGN: This was a historic cohort study of deliveries between 24 and 37 weeks of gestation at the Medical University of South Carolina from 1996 through 2002. Singleton infants who were born to women with preeclampsia were compared with nonpreeclamptic control subjects. The incidence of hyaline membrane disease was compared by chi 2 analysis and Fisher exact test, with significance at a probability value of <.05. Logistic regression analysis was performed to address potential confounders. RESULTS: There were 814 women with preeclampsia and 3021 control subjects. When we controlled for confounding factors, there was a significant increase in the incidence of hyaline membrane disease in the preeclamptic group overall (odds ratio, 1.35; 95% CI, 1.03-1.78). The risk was more pronounced in neonates who were born at 32 weeks of gestation (odds ratio, 1.93; 95% CI, 1.28-2.91). CONCLUSION: The risk of hyaline membrane disease in neonates at < 32 weeks of gestation is increased in patients with preeclampsia. This supports the contention that fetal lung maturity is not accelerated in preeclampsia.     

同步鼻塞间歇正压通气治疗早产儿肺透明膜病的临床研究

目的 评价同步鼻塞间歇正压通气(synchronized nasal intermittent positive pressure venti-lation,SNIPPV)作为初始通气模式治疗早产儿肺透明膜病(hyaline membrane disease,HMD)的临床疗效. 方法 采用前瞻性随机对照研究方法 .选择2008年3月至2009年3月收入我院新生儿重症监护病房的临床诊断HMD的早产儿,应用猪肺磷脂后,对于仍有呼吸困难需无创通气治疗者共42例,随机分为SNIPPV组20例和鼻塞持续正压通气(nasal continuous positive airway pressure,NCPAP)组22例.比较两组上机前后的生命体征、血气分析、无创通气失败率及各种并发症的发生率.两组间比较采用t检验和x~2检验. 结果SNIPPV组上机后3 h及12 h氧分压分别为(78.3±17.6)mm Hg和(83.3±17.7)mm Hg,均高于NCPAP组[分别为(62.5±20.5)mm Hg和(69.6±18.8)mm Hg](P<0.05);二氧化碳分压分别为(42.2±12.2)mm Hg和(41.44±11.2)mm Hg,均低于NCPAP组[分别为(53.74±11.0)mm Hg和(55.3±10.9)mm Hg](P<0.05).SNIPPV组上机后3 h低氧血症及高碳酸血症的发生率分别为5.0%和20.0%,均低于NCPAP组(分别为36.4%和50.0%)(P<0.05),上机后12 h高碳酸血症的发生率也低于NCPAP组(20.0%和59.1%)(x~2=6.654,P=0.010).SNIPPV组无创通气失败率低于NCPAP组(15.0%和45.5%)(x~2=4.456,P=0.033).两组并发症发生率差异无统计学意义.结论 SNIPPV作为应用肺表面活性物质后的初始通气模式治疗早产儿HMD是可行的,且比NCPAP模式更有效.     

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.