重症新生儿肺透明膜病临床病理分析（附19例尸检报告）

目的探讨重症新生儿肺透明膜病透明膜的形成与新生儿存活时间的关系。方法收集经尸检证实的19例重症新生儿肺透明膜病的临床病理资料。结果新生儿存活时间<12小时的8例中有7例肺透明膜呈间隔型,1例呈全肺泡型;存活时间在12～24小时的8例均呈全肺泡型;存活时间～72小时3例中,2例呈间隔型,1例全肺泡型。结论新生儿肺透明膜形成与消散有一个时间演变过程,本病新生儿的死亡率与其合并症密切相关。     

围产期婴儿肺透明膜病

本文报告27例围产期婴儿肺透明膜病的病理学观察和分析。发现肺透明膜形态多种多样,透明膜附着处无上皮存在,讨论了肺透明膜的发生机制。认为呼吸性细支气管,肺泡管和肺泡的基底膜暴露是形成透明膜的重要条件。     

别嘌呤醇对大鼠肾上腺素性肺水肿的影响

本实验采用静脉注射肾上腺素复制的大鼠实验性肺水肿模型,观察了别嘌呤醇对肺水肿的影响。随机将大鼠分为生理盐水组、肾上腺素组和别嘌呤醇+肾上腺素组。结果表明,肾上腺素可使肺血管壁、肺泡壁通透性增高,肺间质、肺泡、支气管水肿,出血及透明膜形成;别嘌呤醇可预防肾上腺素所致肺损伤的发生(P<0.05),延长动物存活时间(P<0.01)。提示肾上腺素性肺水肿的发生与自由基有关。     

新生儿肺透明膜病肺氧合功能和尿量变化相关性

目的: 探讨新生儿肺透明膜病(HMD)机械通气治疗中肺氧合功能和尿量的变化及两者的相关性.方法:对行机械通气治疗的HMD患儿23例按预后情况分存活组和死亡组,观察比较两组动脉血气、动脉/肺泡氧分压比值(PaO2/PAO2)、尿量.结果:存活组PaO2/PAO2、尿量及尿量/入量比值增加,在机械通气48小时、72小时与死亡组比较差异有显著性意义(P＜0.05或0.01).尿量/入量比值存活组于机械通气48小时＞0.8,死亡组至72小时＜0.8.尿量与PaO2/PAO2呈正相关(r=0.4376,P＜0.05).结论:HMD 患儿随着尿量增加肺氧合功能改善,机械通气治疗中密切观察尿量的变化有助于判断预后.     

新生儿特发性呼吸窘迫综合征的预测与防治

<正> 新生儿特发性呼吸窘迫综合征Idiopathic respiratory distress syndrome(下称IRDS),是一个临床诊断名称,指生后不久出现进行性呼吸困难、三凹、青紫和呼吸衰竭,12～72小时病情达高峰。病理以肺泡壁及细支气管壁上附有嗜伊红性透明膜和肺不张为特点,故亦称新生儿肺透明膜病。近年来认为本病的发生与早产低体重儿的肺不成熟、肺表面活性物质缺乏有关。因此,也称本病为未成熟肺及肺表面活性物质缺乏病。其发病多见于     

大白鼠实验性高原肺水肿

正常成年大白鼠在环境温度为5℃左右,经受摸拟5000米高原,72小时后观察到轻度的间质性肺水肿。切除左肺的大白鼠,在摸拟5000米高原,48小时后出现明显的间质性肺水肿。其中部分动物的单个肺泡或局灶肺泡中出现水肿液。 根据组织学检查,在本实验条件下,以间质性肺水肿为主,水肿液漏出部位在肺泡壁毛细血管水平,而后液体聚积在肺泡壁外的血管周围而形成血管周围“袖套”,血管周围水肿可扩展到支气管周围,并形成支气管周围水忡“袖套”。 切除左肺动物比非手术动物表现显著的间质性肺水肿,似可支持在局限性水肿区域肺动脉高压和过度灌流是发生高原肺水肿的主要机制。     

90例新生儿肺透明膜病数字X线摄影床边胸片特征及疗效分析

目的探讨数字X线摄影(DR)床边胸片在新生儿肺透明膜病的诊断及其治疗效果评价中的价值。方法回顾性分析经临床及DR床边胸片证实的新生儿肺透明膜病90例,分析其DR床边胸片特点,治疗后不定期复查DR床边胸片,观察治疗效果。结果依肺泡萎陷程度,X线表现分为四级,90例新生儿肺透明膜病中,Ⅰ级10例,Ⅱ级18例,Ⅲ级45例,Ⅳ级17例,10例Ⅰ级新生儿肺透明膜病患儿经鼻塞持续气道正压通气(CPAP)治疗,并对其中6例胎龄≤32周的患儿使用气管插管注入PS药物治疗,48小时复查DR床边胸片均显示正常;18例Ⅱ级、45例Ⅲ级及17例Ⅳ级新生儿肺透明膜病CPAP及气管内插管注入PS药物治疗后不同时期复查DR床边胸片,76例患儿均有不同程度好转,4例患儿死亡。结论 DR床边胸片对新生儿肺透明膜病的诊断及治疗效果评价具有重要临床参考价值。     

肺泡表面活性物质联合NCPAP治疗新生儿肺透明膜病疗效观察

目的探讨肺泡表面活性物质联合经鼻持续正压通气（NCPAP）治疗新生儿肺透明膜病的疗效及临床价值。方法对我院2011年1月-2013年6月收治的新生儿肺透明膜病患儿（Ⅰ~Ⅲ级）26例,应用肺泡表面活性物质联合NCPAP治疗,观察患儿治疗前后的临床症状、血气分析结果、X线胸片改善情况及并发症发生率,分析其疗效。结果联合NCPAP治疗新生儿肺透明膜病后,其临床症状、血气指标、X线胸片明显改善,并发症少,减少机械通气的概率,治愈率为92.3%。结论 肺泡表面活性物质联合NCPAP治疗新生儿肺透明膜病疗效肯定,提高了早产儿抢救成功率,且方法简单,无创伤,并发症少,预后良好,值得临床推广应用。     

早产儿肺透明膜病应用肺泡表面活性物质联合鼻塞式持续气道正压通气的研究

目的 探讨早产儿肺透明膜病使用肺泡表面活性物质联合鼻塞式持续气道正压通气(NCAPA)的临床疗效.方法 选择2012年1月-2014年5月收治入院的早产儿肺透明膜病患儿40例,随机分为治疗组和对照组各20例,治疗组给予肺泡表面活性物质联合NCAPA治疗,对照组单纯NCAPA治疗,比较2组患儿的临床治疗效果及不良反应情况.结果 治疗组患儿总有效率为95％,明显高于对照组的75％,差异有统计学意义(P＜0.05);治疗1,12,24h后,治疗组血气分析指标均好于对照组(P＜0.05).结论 早产儿肺透明膜病使用肺泡表面活性物质联合NCAPA治疗效果显著,具有一定的临床推广价值.     

新生儿呼吸窘迫综合征3例尸检病理分析

目的提高对新生儿肺透明膜症的认识和诊断水平。方法回顾性分析我院收治的3例新生儿肺透明膜症的临床及尸检病理资料。结果3例中男2例,女1例,分别存活1天、12小时及8小时。2例为剖宫产儿,1例为早产儿,均表现为出生时一般状态良好,出生后6小时内开始出现呼吸困难、全身青紫,抢救无效死亡。尸检病理见肺泡腔、肺泡管和细支气管内弥漫分布的透明膜形成3例,严重急性肺水肿、淤血1例,肝、肾及肾上腺淤血、水肿3例,卵圆孔未闭、动脉导管开放1例。结论新生儿呼吸窘迫综合征为新生儿猝死的主要原因之一,提高对该病的认识,及时向家属解释疾病的发生发展特点,对于减少新生儿死亡率及产科医疗纠纷非常重要。     

狗双后肢高速火器伤后肺组织学和超微结构观察

本研究观察了狗双后肢高速枪弹伤后不同时间内肺组织学和超微结构的改变。结果表明,在伤后0.5h、6h、24h和72h肺脏均出现了不同程度的组织学和超微结构的改变。伤后0.5h和6h,组织学检查可见肺微血管扩张充血,毛细血管破裂,间质和肺泡内出血,局灶性肺不张和肺气肿。伤后24h和72h,除上述改变外,尚可见肺微血管栓塞和透明膜形成。超微结构检查,各组均可见不同程度的肺毛细血管内皮细胞肿胀。Ⅰ型肺泡上皮细胞肿胀,剥脱或变性坏死。Ⅱ型肺泡上皮细胞肿胀,微绒毛变短,数目减少,板层体排空。毛细血管腔内可见白细胞聚集和血小板扣压,白细胞呈明显脱颗粒。此外,本文还对肺损伤的可能机理进行了讨论。     

TREATMENT OF EXPERIMENTAL RESPIRATORY DISTRESS SYNDROME WITH DEXAMETHASONE, SCOPOLAMINE AND ANISODAMINE IN DOGS

38 hybrid dogs were injected intravenously with oleic acid 0.03 mg/kg body weight to induce ex perimental respiratory distress syndrome. The an imals were divided into four groups, one was the control group and the other three groups were treated with dexamethasone, scopolamine hydrobromide and anisodamine. The animals were killed 24 hours after injection. The blood gas parameters of arterial and mixed venous blood were determined before, immediately and 0.5, 1, 2, 4, 6, 22, and 24 hours after oleic acid injection. The average pul- monary arterial pressure was measured hourly. Chest X-rays were taken before and 2, 4, 6, and 24 hours after injection. The histological specimens of the killed animals were examined by light and electron microscopy. It was found that dexame- thasone and anisodamine are effective in treating ex- perimental respiratory distress syndrome while scopo- 1amine is rather disappointing.     

小剂量肝素对大鼠呼吸窘迫综合征肺组织病理及超微结构的影响

探讨了小剂量肝素对呼吸窘迫综合征的治疗作用．将３６只Ｗｉｓｔａｒ大鼠随机分正常组、油酸组、治疗组３组．各组在乌拉坦麻醉下，用微量输液器从股静脉给药物，观察实验的不同时期动脉血氧分压、二氧碳分压和实验１２０ｍｉｎ的肺组织病理学及超微结构的变化．结果，治疗组氧分压下降、二氧化碳分压上升，与油酸组比较较轻，油酸组肺泡壁充血、水肿、坏死、白细胞浸润、肺泡腔内出血、水肿、透明膜形成，而治疗组的肺泡壁及肺泡腔内变化较轻、未见透明膜形成；观察油酸组的超微结构，示肺泡间隔明显增宽，Ⅰ型细胞水肿、坏死，Ⅱ型细胞板层小体排空明显，线粒体嵴排列紊乱及水肿，而治疗组的Ⅱ型细胞板层小体排空及线粒体变化较轻．     

油酸诱发肺损伤犬的早期血液动力学变化

本文观察了油酸诱发肺损伤对早期血液动力学的影响。犬11只,于麻醉、人工通气下获得基础数据后,静注油酸0.1mg/kg,并连续观察血液动力学各项指标,共3小时。油酸注射后,PaO_2进行性下降,肺泡-动脉血氧分压差增大,而供氧能力降低。血液动力学变化表现:心指数逐渐降低,至油酸注射后180分钟仅为对照值的51.7％,心率和心搏指数也同时并行下降。平均动脉压于早期明显降低,继后回升,与对照值无显著差别;平均肺动脉压无显著变化。左室收缩压短暂降低,而左室每捕作功、+dp/dt max、-dp/dt max和阻抗心肌收缩力指数均显著进行性降低。死后肺湿重与体重比值也明显增加。本实验结果提示:(1)油酸肺损伤犬早期表现严重的低氧血症、心输出量降低,心室舒缩功能障碍和组织供氧量降低;(2)心输出量减少可能与心肌收缩力降低有关;(3)实验中未见肺动脉压急剧成倍增加。因此,早期肺损伤的发生非主要由肺微血管静水压增加所致。     

Observations on the Therapeutic Effects of Anisodamine on Respiratory Distress Syndrome

The animal model of dogs was used to study the pathological evolution ofrespiratory distress syndrome (RDS) and the therapeutic effects of anisodaine on the disease.Atotal of 54 dogs were employed and they were divided into control and experimental groups.RDS was inflicted to the dogs by oleic acid injection.Then the clinical manifestations,theblood gas parameters,the pulmonary arterial pressure,the pulmonary wedge pressure,T_3 andT_L,blood cell counts,neutrophil aggregation rate,platelet maximum aggregation rate,TXB_2,6-keto-PGF_(1a) and hemocoagulagrams were obsenved.On the basis of our observations,it is concluded that the complement activities andneutrophil aggregation induced by TXA_2 are likely the initiative factor of RDS,the pathologicalprocess in the lungs is complicated with disseminated intravascular coagulation,and anisodamineexerts certain therapeutic effects on RDS through preventing the cellular membranes andlysosomes from being injured.     

油酸复制狗呼吸窘迫综合征模型的初步观察

本实验取杂种狗9只,其中7只以0.1ml/kg油酸经肺动脉注入造成RDS,于注油酸后2.5、7.5、8.5、9h分别处死,另取2只作为对照。注油酸前后采集动脉血与混合静脉血测定pH、Pao_2、Paco_2、Pvo_2、PEO_2PECO_2计算A-aDo_2Q_s/Q_t。开胸取肺组织进行光镜和电镜检查。结果表明:经肺动脉注入油酸复制成的实验性RDS模型,方法简便可靠。     

Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs

Respiratory distress syndrome was inflicted on 30 dogs with anintravenous injection of oleic acid of the dose 0.06ml/kg. Half of theanimals were treated with anisodamine. Another 5 dogs were injected withsaline to serve as control. The dynamic changes of total hemolyticcomplement activity, neutrophil aggregation rate, platelet aggregation rate,fibrin degradation products, white cell count and platelet count in both theperipheral arterial and venous blood, and blood gas analysis were tested.The pathological and clinical changes were also observed. The results ofthe study suggest that the pathogenesis of respiratory distress syndromewas apparently related to the increase of complement activation, neutrophilaggregating activity, and blood coagulation. The therapeutic effect ofanisodamine can be enhanced if the complement-neutrophil-fibrindegradation products pathway is blocked.     

特普他林对油酸肺损伤后肺水肿的抑制作用

目的 观察特普他林对油酸致伤大鼠肺损伤后肺水肿的影响.方法 随机将大鼠分为正常对照组(C组)、油酸致伤组(I组)和特普他林治疗组(T组),T组于伤后1h经气管滴注特普他林(1×10-4M)溶液5ml/kg.分别于6、12、24h时相点检测总肺水量(TLW)、肺血管外肺水量(EVLW)和肺微血管通透性(PMVP),并同步检测动脉血气参数.结果 油酸致伤后大鼠PMVP 显著增高,TLW和EVLW明显增加, PaO2显著下降;特普他林治疗后,TLW、EVLW和PMVP均较油酸致伤组显著降低(P＜0.01),低氧血症明显改善.结论 特普他林明显降低油酸型肺损伤大鼠的肺微血管通透性和肺含水量,改善换气功能,对急性肺损伤后肺水肿有一定的治疗作用.     

山莨菪碱治疗犬呼吸窘迫综合征肺脏病理观察

本文观察了油酸型犬呼吸窘迫综合征(RDS)对照组和山莨菪碱治疗组肺脏光镜与电镜改变,讨论了RDS的发病机理,认为在RDS的主要病变肺水肿的形成中,有血流动力学因素参与。山莨菪碱对RDS的治疗作用,可能在于其稳定溶酶体膜和对细胞的直接保护作用。尚需进一步研究。     

CI-IANGES IN THE PLASMA LEVELS OF PGE, PGF2a AND 6-Keto-PGFla IN CANINE ENDOTOXIC SHOCK

The plasma levels of PGE, PGF2a and 6-keto PGFla in the canine model of endotoxic shock were determined with radioimmunoassay. Following cndotoxin injection, the PGF2a levels were rapidly increased to peak at 5 minutes. There was a negative correlation between the PGE level and the change in total systemic peripheral resistance at early stage of shock. The administration of anisodamine 2 hours after endotoxin injection showed no effect on the changes of PGE and PGF2a levels in the shocked dogs. The plasma levels of PGE and PGF2a in the shocked children with fulminating epidemic menin gococcal meningitis were also markedly elevated dur- ing shock but fell within normal range at convales- sence. After the dogs were given endotoxin the plasma level of 6-keto-PGFla increased slowly during the first hour, reached a peak at 2 hours and re mained high for 12 hours. There was a negative correlation between the 6keto-PGFla level and the blood pressure. The plasma 6keto PGFla level was decreased and the blood pressure improved corres- pondingly with a negative linear correlation as a result of administration of anisodamine 5-10 minutes after endotoxin injection. These results suggested that PGE and PGI2, as one of the humoral factors, might participate at least partially in the endotoxin induced hypotension, and that the inhibition of PGI2 synthesis was considered contributable to certain degree to the antishock effect of anisodamine.