炎症介质与肺移植缺血再灌注损伤

肺移植为目前治疗终末期肺病的主要手段。随着肺保护技术、手术方法的进步和免疫抑制剂的应用等,肺移植成功率逐年提高,但肺移植术后1年和5年的生存率分别还只有80%和50%左右[1]。原发性移植肺失功为肺移植后早期死亡的首要原因,而缺血再灌注损伤(IRI)是原发性移植肺失功的主要因素。因此,肺移植IRI的分子机制研究对于提高肺移植成功率具有重要意义,受到广泛重视,本文就炎症介质在肺移植IRI中的作用作一综述。     

肺移植前后痰液及支气管分泌物细菌培养和药敏试验结果分析

目的了解肺移植受者肺细菌分布和耐药情况,探讨病原微生物感染对移植肺的影响。方法对本院2003年6月至2005年5月间行肺移植术的12例受者移植前后痰液和支气管分泌物标本进行细菌培养,并对其中阳性标本中的细菌进行鉴定及药敏试验。结果肺移植受者移植前培养出阳性标本8例,其中2例为1种细菌,6例为2种以上的细菌;移植后培养出阳性标本10例,其中4例为1种细菌,6例为2种以上的细菌。肺移植前后共分离出菌株54株,革兰阳性菌占61.1%(33/54),革兰阴性菌占18.5%(10/54),真菌占20.4%(11/54)。分离出的病原菌除对磷霉素、万古霉素较为敏感外,对其他药物均有多药耐药性。结论肺移植受者痰液及分泌物标本的细菌种类及耐药性情况对临床医生在治疗时合理选择抗生素、避免盲目经验用药、及时控制感染有重要意义。     

肺移植后影响患者长期生存的危险因素

背景:国内肺移植开展数量较少,移植后长期生存时间较其他器官移植短,其原因尚不完全清楚。目的:分析影响肺移植后患者长期生存因素。方法:回顾分析61例终末期肺疾病患者接受肺移植的临床资料,根据随访生存时间将患者分为两组。观察组生存时间>3年29例,对照组生存时间<1年32例,对两组患者的一般特征、术式(单、双肺移植)、肺动脉压力、是否应用体外膜氧合等进行多因素逻辑回归分析比较。结果与结论:统计学分析显示,年龄(≥50岁)、肺移植前肺动脉高压、急性排斥和肺部严重感染是影响患者肺移植后长期生存的独立风险因素。提示肺移植治疗终末期肺病,选择合适肺移植患者,移植前控制肺动脉压,移植中严格把握体外膜氧合转流适应证,移植后预防肺部感染,严格免疫抑制剂治疗是延长患者生存时间重要措施。     

肺移植供肺获取100例：冷缺血时间〉6h及肺减容对预后的影响

背景：肺移植过程中供肺获取的手术技巧、冷缺血时间的上限以及供肺与受者胸腔大小不匹配等问题的处理有待进一步研究。目的：总结肺移植中供肺获取的手术技巧,探讨冷缺血时间和肺减容对受者移植后各种并发症以及生存率的影响。方法：回顾分析100例供肺获取和101例受者的临床资料,根据供肺冷缺血时间所有受者分为冷缺血时间〈6h组或〉6h组;另根据移植中是否出现供肺与受者胸腔大小不匹配分为肺减容组和对照组,不匹配的均行不同方式肺减容。分析冷缺血时间〉6h和肺减容对肺移植患者预后的影响。结果与结论：100例供肺获取和101例肺移植均成功,其中1供者的左右肺分别移植给2例受者,共完成101例肺移植。除供肺冷缺血时间〉6h组原发性移植物失功发生率要高于〈6h组（P〈0.05）外,其他各指标差异均无显著性意义（P〉0.05）;肺减容组与对照组各临床指标差异亦无显著性意义（P〉0.05）。提示严格的供者选择、恰当的供肺减容以及尽量缩短供肺冷缺血时间可以有效防止受者移植后各种并发症的发生,提高肺移植成功率,改善患者预后。     

肺移植供肺获取100例:冷缺血时间>6h及肺减容对预后的影响

背景:肺移植过程中供肺获取的手术技巧、冷缺血时间的上限以及供肺与受者胸腔大小不匹配等问题的处理有待进一步研究。目的:总结肺移植中供肺获取的手术技巧,探讨冷缺血时间和肺减容对受者移植后各种并发症以及生存率的影响。方法:回顾分析100例供肺获取和101例受者的临床资料,根据供肺冷缺血时间所有受者分为冷缺血时间<6h组或>6h组;另根据移植中是否出现供肺与受者胸腔大小不匹配分为肺减容组和对照组,不匹配的均行不同方式肺减容。分析冷缺血时间>6h和肺减容对肺移植患者预后的影响。结果与结论:100例供肺获取和101例肺移植均成功,其中1供者的左右肺分别移植给2例受者,共完成101例肺移植。除供肺冷缺血时间>6h组原发性移植物失功发生率要高于<6h组(P<0.05)外,其他各指标差异均无显著性意义(P>0.05);肺减容组与对照组各临床指标差异亦无显著性意义(P>0.05)。提示严格的供者选择、恰当的供肺减容以及尽量缩短供肺冷缺血时间可以有效防止受者移植后各种并发症的发生,提高肺移植成功率,改善患者预后。     

晚期逆行肺灌洗在无心跳供体肺移植中肺保护作用的病理学观察

目的 从病理学角度评价晚期逆行肺灌洗在无心跳供体肺移植中的肺保护作用。方法 健康杂种雄性犬24只,随机分为A、B两组,每组供体、受体犬各6只。建立犬左肺原位移植模型。A组（对照组）行早期肺动脉灌洗联合早期逆行灌洗;B组（晚期逆行肺灌洗组）行早期肺动脉灌洗加早期逆行灌洗再联合晚期逆行灌洗。受体移植后维持机械通气观察6 h。观察移植前供体右肺和移植后6 h供体左肺肉眼观察、光镜及电镜下的不同病理特点。结果 晚期逆行灌洗使供肺灌洗更均匀,颜色更白;光镜下移植前和移植后6 h可见晚期逆行肺灌洗组肺血管内残留的血细胞和微血栓较少,炎症细胞浸润和组织水肿较轻;电镜下移植后6 h可见晚期逆行肺灌洗组肺组织细胞超微结构较为完整,破坏较轻。结论 晚期逆行灌洗可以更好地清除供肺内的微血栓、炎性细胞,减轻缺血及再灌注损伤。     

心脏移植中肺动脉高压的处置

在接受心脏移植的病人中,肺动脉高压对移植心脏的损害已被逐渐认识,它会降低手术疗效。作者对心脏移植病人肺动脉高压的原因、处理方法以及围手术期护理进行了讨论。 为了降低心脏移植病人的病死率,对心脏移植接受者必须进行肺血流动力学监测,以了解是否有肺动脉高压、肺血管阻力（ＰＶＲ）升高,以及通过治疗肺动脉压是否已经降低。肺血流动力学的检查内容包括：收缩期、舒张期和平均肺动脉压,全肺压力梯度和ＰＶＲ。如果肺动脉压高于６．６７ ｋＰａ;ＰＶＲ大于６ ｗｏｏｄ参数;全肺压力梯度大于２．００ｋＰａ,而且对血管扩张剂…     

CRTER杂志“器官移植”栏目关于“心肺移植”的组稿内容（本刊学术部）

心肺移植免疫学.供者心肺的选择、切取及保护.移植手术的麻醉.移植手术体外循环管理.肺移植的远期随访.     

肺移植等待期患者营养知信行调查及影响因素分析

目的调查肺移植等待期患者营养知信行情况,并分析其影响因素,为肺移植围手术期患者开展个体化营养干预提供参考。方法采用便利抽样的方法,选取2018年1—12月在南京医科大学附属无锡人民医院呼吸中心经肺移植评估后等待肺移植的240例患者作为研究对象,采用自制的肺移植等待期患者营养知信行调查问卷进行调查,并分析患者营养知信行的影响因素。结果肺移植等待期患者的营养知识处于一般水平,得分为(18.71±4.53)分;营养态度处于良好水平,得分为(38.00±6.49)分;营养行为处于一般水平,得分为(36.75±4.89)分。多重线性回归结果显示,营养知识的影响因素为经济状况和是否合并神经系统疾病(P<0.05);营养态度的影响因素为职业和血清蛋白(P<0.05);营养行为的影响因素为年龄、文化程度和是否合并泌尿系统疾病(P<0.05)。结论肺移植等待期患者营养知信行水平受到年龄、经济状况、合并疾病情况、职业、文化程度和血清蛋白的影响,在对肺移植患者进行围手术期营养管理时,应充分考虑各类影响因素,针对性地给予精准化的营养干预,通过提高患者的营养知识水平,重点改变其营养态度,最终改善营养行为和营养状况。     

肺移植前后的护理及对患者生活质量的研究

196 3年 ,世界上第 1例肺脏移植手术成功。2 0世纪 80年代初 ,随着免疫抑制药物的出现及外科手术技术的进步 ,肺移植手术的数量迅速增加。目前 ,肺移植已成为越来越多终末期肺病及肺血管疾病患者的外科治疗选择。移植前的护理　患者首先需接受全面的评估 ,以确定其是否符合肺移植手术的标准。由于疾病本身的影响 ,对移植日期的未卜、未来命运的担忧 ,使该期患者常常表现出焦虑与消沉。因此 ,对肺移植前患者护理的目标是 :对患者心理、生理症状、呼吸功能状态和其他相关并发症的护理。 (1)营养。患者的营养状况对肺移植术后并发症的发病率及…     

Antimicrobial effects of lidocaine in bronchoalveolar lavage fluid

The antimicrobial activity of lidocaine in bronchoalveolar lavage fluid (BAL(f)) was investigated. Clinical respiratory isolates were added to BAL(f) suspensions containing lidocaine and to normal saline. The growth of two of four isolates of Streptococcus pneumoniae was significantly reduced in the presence of lidocaine-BAL(f) compared with controls in saline. Growth of Moraxella catarrhalis isolates was reduced in normal saline when compared with BAL(f) containing lidocaine. There was no effect upon the growth of Haemophilus influenzae, Pseudomonas aeruginosa and Candida albicans isolates. The recovery of isolates of S. pneumoniae may be reduced below the critical threshold of 10(5) cfu/mL during bronchoscopy when using lidocaine as a local anaesthetic.     

Biochemical parameters of bronchoalveolar lavage fluid in fat embolism

Objective To identify diagnostic markers distinguishing between acute lung injury/acute respiratory distress syndrome (ALI/ARDS) due to fat embolism syndrome (FES) and that due to other causes, and to investigate whether phospholipase A₂ and platelet-activating factor (PAF) play a role in the pathogenesis of ALI due to FES.Design and setting A prospective study in a 14-bed ICU.Patients We studied 13 patients with FES, 11 with ALI/ARDS from other causes (6 without trauma, ALI/ARDS group 1; 7 with trauma, ALI/ARDS group 2) and 5 without cardiopulmonary disease.Measurements and results We compared broncholveolar lavage (BAL) fluid alterations in the respective groups. Total BAL protein in FES group was significantly higher compared to in ALI/ARDS group 1 and controls but ALI/ARDS group 2. Higher total phospholipids were found than in other groups. The alterations in individual phospholipid classes were similar to those in ALI/ARDS patients. However, total cholesterol, lipid esters, and monoglycerides were significantly higher in FES than in other groups. The level of PAF in FES was significantly higher and there was an inverse correlation between PAF and PAF-acetylhydrolase. Phospholipase A₂ activity was significantly higher in both FES and ALI/ARDS groups than in control.Conclusions The levels of neutral lipids and especially cholesterol and cholesterol esters in BAL can be used to distinguish patients with FES from ALI/ARDS due to other predisposing factors. Phospholipase A₂ may be involved in the development, and PAF-acetylhydrolase in the downregulation of inflammation in FES.     

Surfactant protein A in bronchoalveolar lavage fluid.

We measured surfactant protein A and phosphatidylcholine in the bronchoalveolar lavage fluid from healthy volunteers and several groups of patients with lung diseases to obtain information on surfactant in the lung. We developed three types of enzyme-linked immunosorbent assays that used combinations of polyclonal antiserum and monoclonal antibodies. Phosphatidylcholine was assessed by enzymatic measurement. The median amounts of surfactant protein A in bronchoalveolar lavage fluid determined by the enzyme-linked immunosorbent assay with monoclonal antibodies were as follows: control subjects (n = 10), 2.82 mg/L (range, 0.92 to 5.17 mg/L); patients with asthma (n = 13), 1.89 mg/L (range, 0.45 to 2.95 mg/L); and patients with pulmonary sarcoidosis (n = 20), 2.98 mg/L (range, 0.68 to 7.02 mg/L). The median phosphatidylcholine concentrations in the bronchoalveolar lavage fluid were as follows: control subjects (n = 10), 20 mumol/L (range, 3 to 37 mumol/L); patients with asthma (n = 12), 24 mumol/L (range, 3 to 55 mumol/L); and patients with pulmonary sarcoidosis (n = 20), 26 mumol/L (range, 4 to 76 mumol/L). As a group, the patients with asthma had less surfactant protein A in bronchoalveolar lavage fluid than did the control subjects (Mann-Whitney U test, p less than 0.05). The surfactant protein A levels measured by the enzyme-linked immunosorbent assay with polyclonal antiserum and by a competitive enzyme-linked immunosorbent assay were also lower in bronchoalveolar lavage fluid from patients with asthma than in that from control subjects. The phosphatidylcholine concentrations in all groups were similar.(ABSTRACT TRUNCATED AT 250 WORDS)     

肺泡灌洗液中淋巴细胞表型的测定及临床意义

目的 建立以流式细胞仪（ＦＣＭ）检测肺泡灌洗液（ＢＡＬＦ）中淋巴细胞表型的方法并对其临床意义进行研究。方法 采用ＦＩＴＣ＿ＣＤ４５／ＰＥ－ＣＤ１４设门并结合ＰＩ染色排除非淋巴细胞,细胞碎片等对检测的干扰,以ＦＣＭ分析４３例肺部疾病患者ＢＡＬＦ和对照组外周血淋巴细胞上各怕的表达,并与免疫组化检测方法进行方法学比较。结果 ＦＣＭ法与免疫组化法相关良好,其为精密度远优于免疫组化法。４３例ＢＡＬＦ中Ｔ细胞     

Bronchoalveolar lavage fluid and plasma proteins, chemiluminescence response and protein contents of polymorphonuclear leukocytes from blood and lavage fluid in traumatized patients

The technique of bronchoalveolar lavage was used to obtain serial samples of lavage every two days from non-contused lung areas of seven traumatized patients and four normals; blood was drawn simultaneously. Urea, total protein, albumin, alpha 1-proteinase inhibitor, alpha 2-macroglobulin, lactate dehydrogenase, beta-N-acetyl-glucosaminidase, myeloperoxidase, and elastase enzyme activity, as well as complexed and total elastase concentrations were determined in bronchoalveolar lavage fluids and plasma samples. Lavage fluid cell pattern was counted. Polymorphonuclear leukocytes were isolated from lavage fluids and blood samples. Granulocyte contents of elastase enzyme activity, complexed and total elastase concentrations, and myeloperoxidase and lactate dehydrogenase activity were determined. Polymorphonuclear leukocyte stimulatory functions were measured by luminol-enhanced chemiluminescence. The following results were obtained for the patient group: Patterns of lavage fluid cells were shifted in favour of polymorphonuclear leukocytes and lymphocytes. The protein determinations of bronchoalveolar lavage fluids and plasma samples gave information about the extent of alterations of permeability of the capillary-interstitial-alveolar space (albumin/urea and alpha 1-proteinase inhibitor/urea ratios) as well as about the amounts of cytoplasmic and lysosomal enzymes released by phagocytes (lactate dehydrogenase/urea, beta-N-acetylglucosaminidase/urea, elastase/urea ratios). Polymorphonuclear leukocytes isolated from bronchoalveolar lavage fluids contained a decreased content of myeloperoxidase and elastase enzyme activities and total elastase concentration; the content of complexed elastase was found to be increased more than 100 fold. From chemiluminescence measurements there was evidence for decreased zymosan-induced stimulatory function, while the photon emission rate of polymorphonuclear leukocytes after passage into the alveolar space was increased.     

Detection of tissue kallikrein in the bronchoalveolar lavage fluid of asthmatic subjects.

Kininogenase activity was detected by cleavage of radiolabeled substrate (125I-high molecular weight kininogen [HMWK]) in 22 of 24 bronchoalveolar lavage (BAL) fluid samples from 17 asthmatics who either responded to aerosolized allergen challenge or had symptoms of active asthma. In contrast, six of seven normal controls lacked enzymatic activity. Levels of free immunoreactive kinin found in BAL fluid correlated with the presence of kininogenase activity (P = 0.002). The cleavage pattern of 125I-HMWK by the BAL fluid kininogenase (a dominant 65,000-mol wt fragment), and synthetic inhibitor profile (phe-phe-arg-CH2Cl and phenylmethylsulfonyl fluoride) were compatible with a tissue kallikrein. Peak kininogenase activity eluted at an apparent molecular weight of 20,000-34,000 by HPLC gel filtration. Its antigenic identity was established by immunoblotting with anti-human urinary kallikrein antibody and its activity was inhibited by this antibody. Lysylbradykinin was generated during incubation of fractionated BAL fluid and purified HMWK, the characteristic cleavage product of the tissue kallikreins. We conclude that elevated amounts of tissue kallikrein and kinin are present in the bronchoalveolar spaces of asthmatic subjects. Kinin generation may contribute to the asthmatic response directly through edema formation and smooth muscle contraction and by augmenting release and/or production of preformed (histamine) and secondary mediators such as leukotrienes and platelet-activating factor.