Effect of different ventilation methods combined with pulmonary surfactant on neonatal acute respiratory distress syndrome

BACKGROUND Acute respiratory distress syndrome precipitates is widespread pulmonary injury in impacted individuals,the neonatal respiratory distress syndrome(NRDS),primarily observed in preterm infants,represents a prevalent critical condition in neonatal clinical settings.AIM To investigate the clinical efficacy of various ventilation strategies combined with pulmonary surfactant(PS)therapy in the treatment of NRDS.METHODS A total of 20 neonates diagnosed with respiratory distress syndrome,admitted between May 2021 and June 2022,were randomly assigned to either a research group or a control group.Neonates in the research group received treatment involving high-frequency oscillatory ventilation(HFOV)in conjunction with PS.In contrast,neonates in the control group were administered either controlled mechanical ventilation or synchronous intermittent mandatory ventilation,combined with PS.Arterial blood samples from the neonates in both groups were collected before treatment,as well as 6 h,12 h,24 h,and 48 h post-treatment.These samples underwent blood gas analysis,with measurements taken for pH value,partial pressures of oxygen(O_(2))and carbon dioxide.Concurrently,data was collected on the duration of ventilator use,length of hospitalization time,O_(2) treatment time,treatment outcomes,and complications of the ventilator.RESULTS From 6-48 h post-treatment,both groups demonstrated significant improvements in arterial blood pH and oxygen partial pressure,along with a significant decrease in carbon dioxide partial pressure compared to pre-treatment values(P<0.05).Although these changes progressed over time,there were no significant differences between the two groups(P>0.05).However,the research group had significantly lower X-ray scores,shorter hospitalization time,and less time on O_(2) therapy compared to the control group(P<0.05).Mortality rates were similar between the two groups(P>0.05),but the research group had a significantly lower incidence of complications(P<0.05).CONCLUSION The integration of HFOV combine with PS has proven to effectively expedite the treatment duration,decrease the occurrence of complications,and secure the therapeutic efficacy in managing NRDS.

Osthole attenuates pulmonary arterial hypertension by modulation of phospholipid metabolism

OBJECTIVE Pulmonary arterial hypertension(PAH)is a malignant pulmonary vascular disease lacking efficacy therapeutics.Therefore,it urgently needs to develop safe and effective drugs for PAH treatment.Osthole derived from Cnidium monnieri(L.)Cusson(Shechuangzi)or Angelica pubescens Maxim(Duhuo)has the capacity to alleviate PAH by decreasing pulmonary arterial pressure and alleviating pulmonary vascular remodeling in rats,which is a candidate drug for the prevention of PAH,but the underlying modulatory mechanism is still unclear.Our study aims at investigating the metabolic modulatory mechanism of osthole against PAH employing functional metabolomics strategy.METHODS PAH model rats were successfully established with MCT,following osthole administration,then functional metabolomics based on untargeted metabolomics assay,targeted lipidomics analysis,qRT-PCR,Western blotting and ELISA were performed to investigate the modulatory mechanism of osthole against pulmonary arterial pressure and pulmonary vascular remodeling in PAH.RESULTS Untargeted metabolomics results found that sphingosine 1-phosphate(S1P)was the differential metabolites characterized PAH and reversed by osthole treatment.S1P is a crucial sphingolipid metabolite catalyzed by sphingosine kinases1(Sphk1)and functions as promoting PASMCs proliferation contributing to pulmonary vascular remodeling and pulmonary arterial pressure increase.We revealed that osthole reversed high level of S1P by modulating metabolic enzyme Sphk1 via inactivating microRNA-21-PI3K/Akt/mTOR signal pathway to decrease pulmonary arterial pressure in rats with PAH.Then,targeted phospholipid metabolomics results uncovered that decadienyl-L-carnitine(C10:2)was the differential metabolite characterized PAH and corrected by osthole treatment in rat with PAH.C10:2 is the intermediate metabolite of fatty acid oxidation(FAO),and C10:2 accumulation indicated mitochondrial dysfunction and FAO increase.CONCLUSION Osthole could block lipid metabolic reprogramming through functional modulating the expression of fatty acid translocase,fatty acid synthase,phospholipase A2,carnitine palmitoyltransferase 1A to inhibit C10:2,thus to improve mitochondrial dysfunction and inhibit utilizing lipid to biosynthesize necessary essence for pulmonary artery smooth muscle cells(PASMCs)proliferation.Moreover,we delineated that C10:2 and metabolic reprogramming enzymes were modulated by miRNA-22-3p which was involved in PASMCs proliferation and pulmonary vascular remodeling.Therefore,osthole inhibited miRNA-22-3p mediated lipid metabolic reprogramming to ameliorate pulmonary vascular remodeling.

Early Intratracheal Administration of Corticosteroid and Pulmonary Surfactant for Preventing Bronchopulmonary Dysplasia in Preterm Infants with Neonatal Respiratory Distress Syndrome: A Meta-analysis

There is uncertain result with regard to the use of inhalation or instillation steroids to prevent bronchopulmonary dysplasia in preterm infants. This meta-analysis was designed to evaluate the efficacy and safety of early airway administration (within 2 days after birth) of corticosteroids and pulmonary surfactant (PS) for preventing bronchopulmonary dysplasia (BPD) in premature infants with neonatal respiratory distress syndrome (NRDS). The related studies were retrieved in PubMed, EMBASE, the Cochrane Library, Clinical Trial, CNKI, Wanfang and VIP Database from inception to August 2018. Two reviewers independently screened the studies to ensure that all patients with diagnosis of NRDS were enrolled to studies within 1 day after birth, assessed the quality of included studies by GRADEpro system and extracted the data for review. The meta-analysis was performed by RevMan 5.2 software. A subgroup analysis about inhaled corticosteroid (ICS) delivery method was made between ICS inhalation subgroup [inhalation of ICS by nebulizer or metered dose inhaler (MDI)] and ICS intratracheal instillation subgroup (PS used as a vehicle). Eight randomized controlled trials were enrolled in the meta-analysis, 5 trials of which stated the randomized method, grouping and blinded method, and the follow-up procedures were reported. GRADEpro system showed high quality of 4 trials (5 articles), and the rest 4 trials had moderate quality. Meta-analysis showed that the incidence of BPD was decreased in ICS group, the relative risk (RR) was 0.56 (95% CI: 0.42-0.76), and similar trends were found in ICS inhalation subgroup and ICS intratracheal instillation subgroup, with the corresponding RR being 0.58 (95% CI: 0.41-0.82) and 0.47 (95% CI: 0.24-0.95) respectively. ICS could also significantly reduce the mortality risk as compared with placebo control group (RR: 0.67;95% CI: 0.45-0.99), with RR of ICS inhalation subgroup and ICS intratracheal instillation subgroup being 0.81 (95% CI: 0.34-1.94) and 0.64 (95% CI: 0.41-0.99) respectively. Moreover, the percentage of infants using PS more than one time was lower in ICS group than in the placebo control group, with the RR and 95% CI being 0.55 (95% CI: 0.45-0.67), and that in ICS intratracheal instillation subgroup lower than in ICS inhalation subgroup (RR: 0.56;95% CI: 0.45-0.69, and RR: 0.35;95% CI:0.08-1.52 respectively). There was no significant difference in the incidence of infection or retinopathy of prematurity and neuro-motor system impairment between ICS group and placebo control group, with the corresponding RR being 0.95 (95% CI:0.59-1.52), 0.92 (95% CI: 0.62-1.38) and 1.13 (95% CI: 0.92-1.39), respectively. It was concluded that early administration of ICS and PS is an effective and safe option for preterm infants with NRDS in preventing BPD and reducing mortality, decreasing the additional PS usage, especially for the ICS intratracheal instillation subgroup. Furthermore, the appropriate dose and duration of ICS, combined use of inhalation or instillation of ICS with PS and the long-term safety of airway administration of corticosteroids need to be assessed in large trials.

Surfactant Protein B 1580 Polymorphism Is Associated with Susceptibility to Chronic Obstructive Pulmonary Disease in Chinese Han Population

Summary: Whether surfactant protein B (SP-B)-18A/C and 1580C/T polymorphism were associated with susceptibility to chronic obstructive pulmonary disease (COPD) in Chinese Han population was investigated. After genomic DNA was isolated from blood of COPD smokers and control smokers, the genotypes of SP-B-18A/C and SP-B1580C/T polymorphism loci were determined by polymerase chain reaction-restriction fragment length polymorphism analysis (PCR-RFLP) respectively. The results showed that there was significant difference in genotypes distribution frequency of SP-B1580C/T polymorphism locus between COPD smokers and control smokers. C→T mutation rate (including TT homozygote and CT heterozygote) in COPD smokers was higher than in control smokers (57.9 % vs 41.7 %, χ2=4.93, P<0.05), whereas there was no significant difference in genotypes distribution frequency of SP-B1580-18A/C locus between COPD smokers and control smokers. The allele frequency (29.1 %) of SP-B1580-18A/C locus is lower than T allele (70.9 %) in Chinese Han Population, and the distribution was different from that in Mexican, in which, the A and T allele frequencies were 85 % and 15 % respectively. It was concluded that SP-B1580 T allele was probably associated with increased susceptibility to COPD in Chinese Han population; The polymorphism of SP-B-18A/C locus maybe varied with race.

Pulmonary hypertension and metabolic syndrome: Possible connection, PPARγ and Caveolin-1

A number of disparate diseases can lead to pulmonary hypertension(PH), a serious disorder with a high morbidity and mortality rate. Recent studies suggest that the associated metabolic dysregulation may be an important factor adversely impacting the prognosis of PH. Furthermore, metabolic syndrome is associated with vascular diseases including PH. Inflammation plays a significant role both in PH and metabolic syndrome. Adipose tissue modulates lipid and glucose metabolism, and also produces pro-and anti-inflammatory adipokines that modulate vascular function and angiogenesis, suggesting a close functional relationship between the adipose tissue and the vasculature. Both caveolin-1, a cell membrane scaffolding protein and peroxisome proliferator-activated receptor(PPAR) γ, a ligandactivated transcription factor are abundantly expressed in the endothelial cells and adipocytes. Both caveolin-1 and PPARγ modulate proliferative and anti-apoptotic pathways, cell migration, inflammation, vascular homeostasis, and participate in lipid transport, triacylglyceride synthesis and glucose metabolism. Caveolin-1 and PPARγ regulate the production of adipokines and in turn are modulated by them. This review article summarizes the roles and inter-relationships of caveolin-1,PPARγ and adipokines in PH and metabolic syndrome.

Surfactant Protein A Polymorphism Is Associated with Susceptibility to Chronic Obstructive Pulmonary Disease (COPD) in Chinese Uighur Population

This study investigatedexamined the correlation between surfactant protein-A (SP-A) polymorphism and the susceptibility of cvhronic obstructive pulmonary disease (COPD) in Xinjiang Uighurs. Genomic DNA was extracted from peripheral blood of 194 COPD smokers and 201 healthy smokers of Uighur who were hospitalized in or paid a visit to one of the four Xingjiang-based hospi-tals involved in the study, betweenfrom March 2009 to December 2010. Single nucleotide polymor-phisms (SNPs) were studied on A/G atwithin amino acid aa62 (CCA/CCG rs1136451) and C/T within aa219 (CGG/TGG, rs4253527) in SP-A. Genotypes were determined by using the TaqMan polymerase chain reaction (PCR). Our results showed that genotype frequencies were different be-tween the COPD and normal smokers infor aa62 (χx2=6.852, P=0.033). There were also significant differences in allele genotype frequencies between the COPD and the control and allele G might de-crease the risk COPD (χx2=6.545, P=0.011; OR=0.663; 95% CI: 0.484–0.909). The result suggested We were led to conclude that polymorphism of aa62 (CCA/CCG, rs1136451) of SP-A may be asso-ciated with the susceptibility to COPD in Xingjiang Uighurs.

Metabolic and genetic assessments interpret unexplained aggressive pulmonary hypertension induced by methylmalonic acidemia:A case report

BACKGROUND Pulmonary hypertension (PH) causes significant morbidity and mortality in diverse childhood diseases.However,limited information has been reported to obtain a good understanding of pediatric PH.Gaps exist between genome sequencing and metabolic assessments and lead to misinterpretations of the complicated symptoms of PH.Here,we report a rare case of a patient who presented with severe PH as the first manifestation without significant cardiovascular malformation and was finally diagnosed with methylmalonic aciduria (MMA) after metabolic and genomic assessments.CASE SUMMARY An 11-year-old female presented with an aggressive reduction in activity capability and shortness of breath for only 4 mo and suffered from unexplained PH.A series of examinations was performed to evaluate any possible malformations or abnormalities of the cardiovascular system and lungs,but negative results were obtained.The blood tests were normal except for manifestations of microcytic anemia and elevated total homocysteine.Computed tomography and magnetic resonance imaging failed to identify any pulmonary diseases.Cardiac catheterization examination identified a small right coronary artery to pulmonary artery shunt and severe PH.During the follow-up,PH progressed rapidly.Then,genome sequencing and metabolic disorder screening were performed,which confirmed a diagnosis of MMA with MMACHC c.80A>G/c and 609G> A mutations.Vitamin B12,betaine and bosentan were then administered as the main treatments.During the 6-mo follow-up,the pulmonary artery pressure dropped to 45 mmHg,while the right ventricle structure recovered.The patient’s heart function recovered to NYHA class Ⅱ.Metabolic disorder analysis failed to identify significant abnormalities.CONCLUSION As emerging types of metabolic dysfunction have been shown to present as the first manifestation of PH,and taking advantage of next generation sequencing technology,genome sequencing and metabolic disorder screening are recommended to have a more superior role when attempting to understand unclear or aggressive PH.

Expression of Peroxiredoxins and Pulmonary Surfactant Protein A Induced by Silica in Rat Lung Tissue

Silicosis is one of the most serious occupational diseases in China and dates back to centuries ago. In this study, we successfully established a rat model of silicosis by intratracheal silica injection for 28 days and determined hydroxyproline levels to evaluate collagen metabolism in lung homogenates. Oxidative stress status was evaluated by detecting catalase and glutathione peroxidase activities.

Vascular Metabolic Mechanisms of Pulmonary Hypertension

Pulmonary hypertension(PH)is a severe and progressive disease characterized by increased pulmonary vascular resistance leading to right heart failure and death.In PH,the cellular metabolisms including those of the three major nutrients(carbohydrate,lipid and protein)are aberrant in pulmonary vascular cells.Glucose uptake,glycolysis,insulin resistance,sphingolipid S1P,PGE2,TXA2,leukotrienes and glutaminolysis are upregulated,and phospholipid-prostacyclin and L-arginine-nitric oxide pathway are compromised in lung vascular cells.Fatty acid metabolism is disordered in lung endothelial cells and smooth muscle cells.These molecular mechanisms are integrated to promote PH-specific abnormal vascular cell proliferation and vascular remodeling.This review summarizes the recent advances in the metabolic reprogramming of glucose,fatty acid,and amino acid metabolism in pulmonary vascular remodeling in PH and the mechanisms for how these alterations affect vascular cell fate and impact the course of PH.

Functional changes of pulmonary surfactant in rats with lung injury induced by endotoxin

We studied the functional changes of pulmonary surfactant （PS） in acutelung injury models produced by endotoxin injection (E.coli O55B5) in rats.The sur-face properties of the lung lavage liquid and the total phospholipids （TPL） ex-tracted from it were assessed on a modified Wilhelmy film balance.γ-A isothermof the lavage liquid revealed an increase in minimum surface tension and a de-crease in hysteresis area,recruitment index and stability index,whereas that ofTPL extracted from it did not show any change except for hysteresis area.Thesurface activity correlates positively with the TPL content but negatively with thetotal protein content in the lavage liquid.The findings indicated that there was adysfunction of PS in rats with the lung injury induced by endotoxin,suggestingthat the function deficiency of PS might be caused by decreased phospholipidsand increased proteins in the alveoli.

Intervention effect of Danbei Yifei formula on pulmonary fibrosis based on urine metabolomics by UHPLC-Q-Exactive

Objective:Determine the urinary biomarkers and pathogenesis of pulmonary fibrosis rats,and elaborate the intervention mechanism of DanBei YiFei formula.Methods:Bleomycin was injected into the trachea to induce pulmonary fibrosis in rats after anesthesia,and the diagnostic indexes of clinical pulmonary fibrosis,including superoxide dismutase,glutathione and malondialdehyde,were measured.High-throughput metabolic data of rats with pulmonary fibrosis were obtained by the latest high-resolution liquid-mass spectrometry technology,the multidimensional data were processed by Chemometrics algorithm to screen biomarkers related to pulmonary fibrosis.While,metabolic function indexes of rats after administration was observed,and the effective mechanism of DanBei YiFei formula on pulmonary fibrosis was expounded.Results:The clinical biochemical indexes showed that there were significant differences in metabolism in the model group,which confirmed the success of the preparation of the model of pulmonary fibrosis.Metabolisms research showed that the metabolic contour of the rats with pulmonary fibrosis was found to be significantly deviated,and the metabolism in vivo was abnormal.After the DanBei YiFei formula was given,the overall metabolic contour of the rats showed a trend of back modulation,and developed in the direction of healthy rats.With database matching and data processing 12 biomarkers,including Fumaric acid,Arginine and Spermidine,were obtained which were radically different from those of healthy rats and pulmonary fibrosis rats.Conclusion:DanBei YiFei formula has definite therapeutic effect on pulmonary fibrosis rats.Regulation of Tricarboxylic acid cycle and Arginine metabolic pathway may be the mechanism of its treatment of pulmonary fibrosis.

Morphofunctional Characteristics of Pulmonary Surfactant System and Its Effect on Immune Cells in Influenza A (H1N1) Pathogenesis

There is an annual increase of influenza-related SARI cases in winter months. Despite the high relevance of this problem, influenza pathogenesis and the role of surfactant system and its SP-A (surfactant protein A) enzyme in antiviral defense remain poorly understood. SP-A activates macrophage M1 polarization and triggers an antiviral response due to the activation of T-cells and dendritic cells. Therefore, surfactant system is an important element of infection protection and a promising therapeutic target.

Correlation of neonatal pulmonary surfactant protein A gene polymorphism with pneumonia susceptibility and inflammatory response

Objective:To study the correlation of neonatal pulmonary surfactant protein A gene polymorphism with pneumonia susceptibility and inflammatory response.Methods:Neonates who were born and diagnosed with pneumonia in Zigong Maternity and Child Healthcare Hospital between September 2015 and February 2017 were selected as pneumonia group, and neonates without infection were selected as control group. SP-A gene rs1059054 and rs1136454 loci polymorphism, the contents of inflammatory cytokines in serum as well as the expression of inflammatory transcription factors in peripheral blood were determined.Results:The constituent ratio of rs1059054 loci CC genotype of pneumonia group was significantly higher than that of control group while the constituent ratio of CT and TT genotypes were significantly lower than those of control group;the constituent ratio of rs1136454 loci AA genotype was significantly lower than that of control group while the constituent ratio of AG and GG genotypes were significantly higher than those of control group. PCT, sTREM1, TNF-α and IL-6 levels in serum as well as RORγt mRNA expression in peripheral blood of pneumonia children with SP-A gene rs1059054 loci CC genotype were significantly higher than those of pneumonia children with CT genotype and TT genotype while SOCS1 and Foxp3 mRNA expression in peripheral blood were significantly lower than those of pneumonia children with CT genotype and TT genotype;PCT, sTREM1, TNF-α and IL-6 levels in serum as well as RORγt mRNA expression in peripheral blood of pneumonia children with SP-A gene rs1136454 loci AA genotype were significantly lower than those of pneumonia children with AG genotype and GG genotype while SOCS1 and Foxp3 mRNA expression in peripheral blood were significantly higher than those of pneumonia children with AG genotype and GG genotype.Conclusion: Neonatal SP-A gene rs1059054 loci CC genotype can increase the pneumonia susceptibility and aggravate inflammatory response, and rs1136454 loci AA genotype can decrease pneumonia susceptibility and relieve inflammatory response.

Study on Pulmonary Surfactant of Sudden Death of Infant

Objective To find the pathogenesis of sudden infant death syndrome (SIDS) from changes of pulmonary surfactant. Methods By means of thin layer chromatography technique, surfactant in whole lung specimens of 10 infants with SIDS and 10 control infants without SIDS (dead of nonrespiratory diseases) were examined qualitatively and quantitatively. Results Eleven components in pulmonary surfactant were examined qualitatively, including lysophosphatidylcholine, sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, phosphatidic acid, cholesterol and neutral lipids. Quantitative examination showed that the amount of surfactant of whole lung specimens in sudden death group [(8.9±1.0) mg/g wet lung weight] was significantly less than that in control group [(12.6±1.4) mg/g wet lung weight, P<0.01]. Qualitative variance showed that the percentages of phosphatidylcholine (49.4%±2.0%) and phosphatidylglycerol (2.6%±0.7%) decreased markedly in sudden death group compared with those in control group (61.5%±3.0% and 4.3%±1.5%, P<0.01). Conclusion Before death there is serious defect on metabolism of pulmonary surfactant in sudden death infants, with the amount decreasing and the ratio of its components being disturbed, which is one of the important pathogenies of SIDS.

注射用牛肺表面活性剂不同给药方式在新生儿胎粪吸入综合征中的应用

目的探讨注射用牛肺表面活性剂不同给药方式在新生儿胎粪吸入综合征(MAS)中的应用效果。方法回顾性分析2021年3月至2023年3月南阳市第一人民医院收治的120例MAS患儿的临床资料,根据给药方式不同分为A组和B组各60例。A组患儿采用肺泡灌洗+气管内滴入给药,B组患儿采用气管内滴入给药,连续治疗48 h。比较两组患儿的临床疗效,以及治疗前后的血气指标[氧分压(PaO_(2))、二氧化碳分压(PaCO_(2))、氧指数(OI)]、肺动脉收缩压(SPAP)、凝血纤溶指标[D-二聚体(D-D)、纤溶酶原激活抑制剂-1(PAI-1)/组织型纤溶酶原激活物(t-PA)、血小板活化因子(PAF)]、炎症因子[肿瘤坏死因子-α(TNF-α)、降钙素原(PCT)、白细胞介素-5(IL-5)、白细胞介素-13(IL-13)]水平,同时比较两组患者的康复相关指标和并发症发生情况。结果A组患儿的治疗总有效率为91.67%,明显高于B组的76.67%,差异有统计学意义(P<0.05);治疗后,A组患儿的PaO_(2)为(60.65±6.33)mmHg,明显高于B组的(56.12±5.93)mmHg,PaCO_(2)、OI、SPAP分别为(42.36±4.02)mmHg、13.10±1.12、(26.14±2.67)mmHg,明显低于B组的(45.66±4.33)mmHg、(15.66±1.53)、(29.46±3.11)mmHg,差异均有统计学意义(P<0.05);治疗后,A组患儿的血浆D-D、PAI-1/t-PA、PAF含量分别为(1.35±0.38)mg/L、3.52±0.78、(404.55±78.78)×10^(9)/L,明显高于B组的(1.00±0.31)mg/L、2.64±0.71、(340.59±65.33)×10^(9)/L,差异均有统计学意义(P<0.05);治疗后,A组患儿的血清TNF-α、PCT、IL-5、IL-13含量分别为(11.11±1.01)ng/L、(0.78±0.23)ng/mL、(0.90±0.34)pg/mL、(1.15±0.66)pg/mL,明显低于B组的(13.75±1.63)ng/L、(1.46±0.34)ng/mL、(1.50±0.40)pg/mL、(1.63±0.94)pg/mL,差异均有统计学意义(P<0.05);A组患儿的发绀、吸气性三凹征消失时间及氧疗时间、住院时间、机械通气时间明显短于B组,差异均有统计学意义(P<0.05);A组患者的并发症总发生率为1.67%,明显低于B组的15.00%,差异有统计学意义(P<0.05)。结论相较于气管内滴入给药,注射用牛肺表面活性剂肺泡灌洗+气管内滴入给药治疗MAS患儿的治疗效果更优,其可促进血气指标、凝血纤溶指标恢复,降低肺动脉高压,减轻机体炎性损伤,降低并发症发生率。

肺泡灌洗术联合肺表面活性物质治疗1例儿童外源性脂质性肺炎并文献复习

目的:探讨经支气管镜肺泡灌洗术联合肺表面活性物质治疗1例儿童外源性脂质性肺炎的应用价值。方法:收集我院收治的1例外源性脂质性肺炎患儿的临床诊疗资料,并进行文献分析。结果:患儿意外吸入油性稀释液体后出现咳嗽、气促进行性加重,血氧饱和度降低,血炎症指标增高,胸部计算机断层扫描(CT)见双肺多发性病变,确诊外源性脂质性肺炎后及时予以经支气管镜肺泡灌洗术,并首次联合应用肺表面活性物质经支气管镜注入治疗,同时予以无创正压机械通气、抗感染、糖皮质激素雾化等治疗。治疗后,患儿咳嗽、气促、低氧血症等临床表现及胸部影像学短期内明显好转。结论:儿童外源性脂质性肺炎早期应用经支气管镜肺泡灌洗术联合肺表面活性物质治疗临床疗效好,有较大临床推广价值。

初诊慢性阻塞性肺疾病伴高压病临床症状、生存质量及实验室指标研究

目的探讨初诊慢性阻塞性肺疾病(COPD)伴高血压患者呼吸道症状、生存质量、血常规及外周血骨代谢指标特征及意义。方法选取2019年1月至2022年4月在我院治疗的初诊COPD伴高血压患者92例作为观察组,同时选取初诊无高血压的COPD患者92例作为对照组,比较两组改良版英国医学研究委员会呼吸问卷(mMRC)、COPD患者自我评估测试问卷(CAT)、COPD全球倡议(GOLD)、SF-36量表评分、血常规及骨代谢指标差异。结果观察组mMRC评级≥2级的比例、CAT评分明显高于对照组(P<0.05),而SF-36评分明显低于对照组(P<0.05)。观察组GOLD分级明显高于对照组(P<0.05),用力肺活量(FVC)和第一秒呼气量(FEV_(1))明显低于对照组(P<0.05)。观察组和对照组白细胞计数(WBC)、中性粒细胞计数(NEUT)、淋巴细胞计数(LYM)等比较差异无统计学意义(P>0.05);观察组股骨颈骨密度、血钙水平明显低于对照组(P<0.05),而甲状旁腺激素(PTH)和骨钙素(BGP)水平明显高于对照组(P<0.05)。观察组C反应蛋白(CRP)、降钙素原(PCT)、白细胞介素(IL)-6、IL-4和IL-10明显高于对照组(P<0.05)。观察组高血压分级与mMRC评级、CAT评分和GOLD分级呈正相关(r_(s)=0.455、0.302、0.501,P<0.05),而与FVC、FEV1呈负相关(r_(s)=-0.311、-0.334,P<0.05)。结论初诊COPD伴高血压病患者呼吸症状较重,生存质量较差,发生骨质疏松风险增加,同时患者血压情况与呼吸症状程度有一定关系。

脂肪酸代谢重编程在肺纤维化中的研究进展

肺纤维化是一类进行性间质纤维化性肺部疾病,死亡率高。其发病机制复杂,涉及脂肪酸的代谢重编程,包括脂肪酸的从头合成、摄取、氧化以及衍生物的改变。脂肪酸代谢重编程参与调控肺泡上皮细胞的生存状态、巨噬细胞极化类型以及成纤维细胞活化情况,发挥促进或者抑制肺纤维化的作用。通过判断或干预脂肪酸代谢重编程相关过程可以有效预防、诊断和治疗肺纤维化。

肺动脉高压生物标志物研究进展

肺动脉高压是一种发病机制尚未阐明的心肺血管疾病,其特征是肺小动脉进行性闭塞性血管病变,发病率和病死率均较高。多数患者发现时已出现右心功能不全,进展至疾病终末期,因此,早发现、早诊断、早治疗对肺动脉高压患者的生存期延长和生活质量的提高尤为重要。生物标志物可用于客观评估肺动脉高压生理和病理过程及治疗效果的监测,其对肺动脉高压早期诊断和预后评估起着重要作用。该文从炎症标志物、免疫标志物、转录调控、氧化应激、代谢物、血栓标志物、右心室重塑标志物等方面对肺动脉高压的生物标志物做一综述。

早期联合应用外源性PS和iNO治疗PPHN的效果

目的探讨早期联合应用外源性肺表面活性物质(PS)和吸入一氧化氮(iNO)治疗新生儿持续性肺动脉高压(PPHN)的效果。方法选取2019年1月1日至2021年12月31日收治的100例PPHN患儿为研究对象,按照随机数字表法将其分成对照组和观察组,各50例。对照组应用iNO+安慰剂(空气),观察组应用iNO+外源性PS。比较两组的治疗效果。结果治疗前,两组的肺动脉收缩压(PASP)、氧分压(PaO_(2))、二氧化碳分压(PaCO_(2))、pH及氧合指数(OI)比较,差异无统计学意义(P>0.05);治疗24、48 h后,两组的PASP、PaCO_(2)、OI均降低,PaO_(2)及pH均升高,且观察组优于对照组,差异具有统计学意义(P<0.05)。观察组的治愈率明显高于对照组,应用体外氧合膜肺(ECMO)及死亡率低于对照组,呼吸机使用时间及总住院时间短于对照组,差异具有统计学意义(P<0.05);两组的不良反应发生情况比较,差异无统计学意义(P>0.05)。结论早期联合应用外源性PS和iNO可明显改善PPHN患儿的氧合情况、降低PASP,减少呼吸机使用时间、总住院时间、对ECMO需求及死亡率,值得临床推广应用。