老年支气管哮喘患者血清MC-CP、Th17的表达及其与呼吸功能、肺功能的相关性分析

摘要 目的：探究老年支气管哮喘患者血清肥大细胞羧肽酶（MC-CP）、Th17表达及其与患者呼吸功能、肺功能的相关性。方法：选择2018年4月至2021年8月于中国人民解放军东部战区总医院接受治疗的120例老年支气管哮喘患者为研究组（SG）,另选同期于我院接受治疗的100例支气管炎患者为对照组（CG）,对比两组患者血清MC-CP、Th-17、呼气峰值流速（PEF）、第1秒用力呼气量（FEV₁）、血氧分压（PaO₂）、FEV₁占预计值的百分数（FEV₁/FVC）差异,就研究组患者MC-CP、Th-17水平与其呼吸功能、肺功能的相关性开展Spearman分析。结果：（1）研究组患者的MC-CP水平明显高于对照组,Th17百分比同样明显高于对照组（P<0.05）;（2）研究组患者的呼吸功能指标PEF、PaO₂,以及肺功能指标FEV₁、FEV₁/FVC均明显低于对照组（P<0.05）;（3）研究组患者MC-CP与PEF、PaO₂呈现明显负相关联系（r=-0.558、-0.700,P<0.001）,研究组患者Th17与PEF、PaO₂呈现明显负相关联系（r=-0.695、-0.774,P<0.001）;（4）研究组患者MC-CP与FEV₁、FEV₁/FVC呈现明显负相关联系（r=-0.609、-0.481,P<0.001）,研究组患者Th17与FEV₁、FEV₁/FVC呈现明显负相关联系（r=-0.622、-0.561,P<0.001）。结论：老年支气管哮喘患者血清MC-CP及Th17水平会出现异常升高状态,而呼吸功能与肺功能会出现降低,相关性分析显示此类患者血清MC-CP及Th17水平与其呼吸功能、肺功能均呈现负相关联系。     

BiPAP正压无创呼吸机辅助治疗老年AECOPD的临床疗效及对患者肺功能、血清炎性因子和预后指标的影响

摘要 目的：观察双水平正压无创通气（bi-level positive airway pressure,BiPAP）辅助治疗老年慢性阻塞性肺疾病急性加重期（Acute Exacerbation of Chronic Obstructive Pulmonary Disease,AECOPD）的临床疗效以及患者治疗前后肺功能、血清炎性因子和预后指标的变化。方法：选择本院在2017年8月至2020年7月期间收治的150例AECOPD患者,采用随机数字表法分为对照组和研究组,每组75例。给予两组抗感染、祛痰、纠正水电解质紊乱、营养支持等基础治疗,在此基础上给予对照组患者低流量吸氧治疗,给予研究组患者选择合适面罩进行BiPAP治疗。比较两组治疗总有效率以及治疗前和治疗后肺功能指标[1 s用力呼气量（1 s forced expiratory volume,FEV₁）、FEV₁/用力肺活量（FEV₁/forced vital capacity,FEV₁/FVC）和FEV1占预计值百分比（FEV₁ as a percentage of predicted value,FEV₁%）]、血气指标[动脉血氧分压（Arterial partial pressure of oxygen,PaO₂）和动脉二氧化碳分压（arterial partial pressure of carbon dioxide,PaCO₂）]、血清炎性因子[白细胞介素-6（Interleukin-6,IL-6）、IL-8和肿瘤坏死因子α（TNF-α）水平]、可溶性髓样细胞触发受体-1（soluble triggering receptor expressed on myeloid cells-1,sTREM-1）以及全身性炎症反应综合征（systemic inflammatory response syndrome,SIRS）量化评分。结果：研究组和对照组患者治疗总有率分别为92.00 %和74.67 %（P<0.05）。两组治疗后FEV₁、FEV₁/FVC、FEV₁%、PaCO₂、SIRS评分以及血清IL-6、IL-8、TNF-α和sTREM-1水平都明显低于治疗前,PaO₂明显高于治疗前（P<0.05）。研究组治疗后FEV₁、FEV₁/FVC、FEV₁%、PaCO₂、SIRS评分以及血清IL-6、IL-8、TNF-α和sTREM-1水平都明显低于对照组,PaO₂明显高于对照组（P<0.05）。结论：BiPAP能够提高老年AECOPD患者临床疗效,改善肺功能、血气水平和预后,缓解炎症状态。     

AECOPD合并PH患者血清Hcy、Cys-C水平与肺功能、动脉血气分析指标及肺动脉收缩压的关系研究

摘要 目的：探究慢性阻塞性肺疾病急性加重期（AECOPD）合并肺动脉高压（PH）患者血清同型半胱氨酸（Hcy）、胱抑素C（Cys-C）水平与肺功能、动脉血气分析指标及肺动脉收缩压的关系。方法：选择2017年12月至2019年12月我院诊治的80例AECOPD合并PH患者作为AECOPD合并PH组。同时选择80例AECOPD未合并PH患者作为单纯AECOPD组以及50名在我院进行体检的健康志愿者作为健康组。检测并比较各组受试者的血清Hcy和Cys-C水平、第一秒用力呼气容积占用力肺活量比值(FEV₁/FVC）、动脉氧分压（PaO₂）、第一秒用力呼气容积占预计值的百分比（FEV₁%pred）、动脉二氧化碳分压（PaCO₂）,肺动脉收缩压（PASP）,分析各指标的相关性。结果：AECOPD合并PH组血清Hcy、Cys-C水平以及PASP最高,其次为单纯AECOPD组,健康组最低（P<0.05）。健康组FEV₁%pred、FEV₁/FVC最高,其次为单纯AECOPD组,AECOPD合并PH组最低（P<0.05）。与单纯AECOPD组相比,AECOPD合并PH组PaO₂明显下降,PaCO₂明显升高（P<0.05）。经Pearson相关性分析可得,血清Hcy和Cys-C与FEV₁%pred、FEV₁/FVC和PaO₂均呈负相关（P<0.05）,而与PaCO₂和PASP均呈正相关（P<0.05）。结论：血清Hcy和Cys-C水平异常升高与AECOPD患者并发PH相关,并且与AECOPD合并PH患者肺功能下降、动脉血气异常以及PASP异常升高存在相关性。     

经鼻高流量加温湿化吸氧联合丹参注射液治疗AECOPD合并轻度Ⅱ型呼吸衰竭的效果及对血气、肺功能的影响分析

摘要 目的：探讨经鼻高流量加温湿化吸氧联合丹参注射液治疗慢性阻塞性肺疾病急性加重期（AECOPD）合并轻度Ⅱ型呼吸衰竭的效果及对患者血气、肺功能的影响。方法：按照随机数字表法将本院重症医学一科在2020年3月至2023年2月期间收治的88例AECOPD合并轻度Ⅱ型呼吸衰竭患者分为对照组和观察组,各44例。两组均采用经鼻高流量加温湿化吸氧治疗,在此基础上给予观察组患者丹参注射液滴注。比较两组患者临床疗效以及治疗前后血气指标[动脉血氧分压（PaO₂）和动脉二氧化碳分压（PaCO₂）]、肺功能指标[1 s用力呼气量（FEV₁、FEV₁/用力肺活量（FEV₁/FVC）和FEV₁占预计值百分比（FEV₁%）]、炎性因子[白介素6（IL-6）、IL-8、肿瘤坏死因α（TNF-α）]和血清生化指标[转化生长因子β1（TGF-β1）、内皮素-1（ET-1）、缔组织生长因子（CTGF）]水平。结果：（1）观察组总有效率高于对照组（P＜0.05）。（2）两组治疗后PaO₂显著增加,PaCO₂显著降低（P<0.05）,观察组治疗后PaO₂较对照组高,PaCO₂较对照组低（P<0.05）。（3）两组治疗后FEV₁、FEV₁/FVC、FEV₁%均显著增加（P<0.05）。观察组患者较对照组高（P<0.05）。（4）两组治疗后血清IL-6、IL-8和TNF-α水平均显著降低（P<0.05）。观察组患者治疗后较对照组低（P<0.05）。（5）两组治疗后血清TGF-β1、ET-1和CTGF水平均显著降低（P<0.05）。观察组患者治疗后血清TGF-β1、ET-1和CTGF水平均显著低于对照组（P<0.05）。结论：结论：经鼻高流量加温湿化吸氧联合丹参注射液治疗AECOPD合并Ⅱ型呼吸衰竭疗效肯定,改善患者血气和肺功能,减轻炎性反应。     

支气管哮喘患者血清miR-29a-3p、miR-98-5p表达水平与肺功能、气道炎症和糖皮质激素治疗敏感性的关系研究

摘要 目的：探讨支气管哮喘（BA）患者血清微小核糖核酸（miR）-29a-3p、miR-98-5p表达水平与肺功能、气道炎症和糖皮质激素（GC）治疗敏感性的关系。方法：选取2020年1月～2022年1月潍坊市人民医院收治的150例BA患者为BA组,根据BA患者GC治疗敏感性将其分为抵抗组43例和敏感组107例,另选取同期57名体检健康者为对照组。收集BA组、对照组肺功能和气道炎症指标资料,采用实时荧光定量逆转录聚合酶链式反应（qRT-PCR）检测两组血清miR-29a-3p、miR-98-5p表达水平。通过Spearman相关性分析BA患者血清miR-29a-3p、miR-98-5p表达水平与肺功能和气道炎症指标的相关性,单因素和多因素Logistic回归分析BA患者GC治疗抵抗的影响因素。结果：与对照组比较,BA组血清miR-29a-3p、miR-98-5p表达水平和第1秒用力呼气容积占预计值百分比（FEV₁％）、第1秒用力呼气容积/用力肺活量（FEV₁/FVC）、峰值呼气流速（PEF）降低,呼出气一氧化氮（FeNO）水平升高（P均＜0.05）。Spearman相关性分析显示,BA患者血清miR-29a-3p、miR-98-5p表达水平与FEV₁％、FEV₁/FVC、PEF呈正相关,与FeNO水平呈负相关（P均＜0.05）。单因素分析显示,抵抗组体质指数＞24 kg/m²、吸烟比例高于敏感组,血清miR-29a-3p、miR-98-5p表达水平低于敏感组（P＜0.05）。多因素Logistic回归分析显示,体质指数＞24 kg/m²、吸烟为BA患者GC治疗抵抗的独立危险因素,血清miR-29a-3p、miR-98-5p表达水平升高为其独立保护因素（P均＜0.05）。结论：BA患者血清miR-29a-3p、miR-98-5p水平降低,与肺功能下降、气道炎症和GC治疗抵抗有关。     

血清钙结合蛋白S100A12、脂联素及IL-17与稳定期COPD患者严重程度及肺功能的相关性

摘要 目的：探讨血清钙结合蛋白S100A12、脂联素及白细胞介素-17（Interleukin-17,IL-17）水平与稳定期慢性阻塞性肺疾病（COPD）病情严重程度和肺功能的关系。方法：选择稳定期COPD患者（稳定期COPD组）和健康体检者（对照组）各80例,稳定期COPD患者分为四级：I级轻度（22例）,Ⅱ级中度（24例）,Ⅲ级重度（19例）,Ⅳ级极重度（15例）。使用肺功能仪对所有研究对象的肺功能进行检查,采用血气分析仪检测动脉血中的氧分压 (PaO₂) 和二氧化碳分压 (PaCO₂),采用酶联免疫吸附试验检测血清中钙结合蛋白S100A12、脂联素和IL-17水平,采用 Pearson相关分析各指标之间的相关性。结果：稳定期COPD组肺功能[第一秒用力呼出气量容积占预计值百分比（FEV₁%）和第一秒用力呼出气量容积/用力肺活量（FEV1/FVC%）]和PaO₂显著低于对照组（P<0.05）,并随着COPD严重程度增加而降低（P<0.05）;稳定期COPD组血清钙结合蛋白S100A12、脂联素、IL-17水平和PaCO₂均高于对照组（P<0.05）,并随COPD严重程度增加而升高（P <0.05）。Pearson相关分析显示：稳定期COPD患者血清钙结合蛋白S100A12、脂联素和IL-17水平与FEV₁%、FEV₁/FVC%和PaO₂呈负相关（P<0.05）,与PaCO₂呈正相关（P<0.05）。结论：钙结合蛋白S100A12、脂联素和IL-17可能共同参与了稳定期COPD慢性炎症过程,引起气流受限,影响肺通气功能,可以辅助评估稳定期COPD病情的严重程度。     

单吸入器三联疗法联合肺早期康复运动训练治疗中重度慢性阻塞性肺疾病患者的临床研究

摘要 目的：探讨单吸入器三联疗法联合肺早期康复运动训练治疗中重度慢性阻塞性肺疾病（COPD）患者的临床研究。方法：根据随机数字表法，将汕头大学医学院第二附属医院2022年7月-2023年1月间收治的84例中重度COPD患者分为对照组（42例，单吸入器三联疗法治疗）和实验组（42例，对照组的基础上接受肺早期康复运动训练治疗）。观察并对比两组的肺功能指标[用力肺活量（FVC）、第一秒用力呼气容积（FEV₁）、FEV₁/FVC]、血气分析指标[血氧饱和度（SaO₂）、动脉血氧分压（PaO₂）、动脉血二氧化碳分压（PaCO₂）]、6分钟步行距离（6MWD）、COPD评估测试（CAT）评分、治疗期间急性加重频率、血清炎症因子[肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）、C反应蛋白（CRP）]。结果：治疗后，实验组FEV₁、FVC、FEV₁/FVC高于对照组（P<0.05）。治疗后，实验组PaCO₂低于对照组，PaO₂、SaO₂高于对照组（P<0.05）。治疗后，实验组6MWD高于对照组，CAT评分、治疗期间急性加重频率低于对照组（P<0.05）。治疗后，实验组血清TNF-α、IL-6、CRP水平低于对照组（P<0.05）。结论：单吸入器三联疗法联合肺早期康复运动训练治疗中重度COPD患者，可增强运动耐力，提高生活活动能力，减少治疗期间疾病急性加重频率，同时还可改善血气分析和肺功能指标，降低血清炎症因子水平。     

老年慢性阻塞性肺疾病急性加重期患者血清CTRP-4、CTRP-6、CTRP-9与肺功能和炎症因子的相关性分析

摘要 目的：探讨老年慢性阻塞性肺疾病急性加重期（AECOPD）患者血清补体C1q/肿瘤坏死因子相关蛋白4（CTRP-4）、CTRP-6、CTRP-9与肺功能和炎症因子的相关性。方法：选取2020年1月～2022年1月我院收治的117例AECOPD患者为AECOPD组,72例慢性阻塞性肺疾病稳定期（SCOPD）患者为SCOPD组,另选取同期58例体检健康者为对照组。采用酶联免疫吸附法检测血清CTRP-4、CTRP-6、CTRP-9水平,通过Pearson/Spearman相关性分析老年AECOPD患者血清CTRP-4、CTRP-6、CTRP-9与肺功能指标[第1秒用力呼气容积占预计值百分比（FEV₁％）、第1秒用力呼气容积/用力肺活量（FEV₁/FVC）]和炎症因子[白细胞介素（IL）-1β、IL-6、IL-8、肿瘤坏死因子-α（TNF-α）]的相关性。结果：对照组、SCOPD组、AECOPD组血清CTRP-4水平依次升高,CTRP-6、CTRP-9水平依次降低（P＜0.05）。老年AECOPD患者血清CTRP-4水平与FEV₁％、FEV₁/FVC呈负相关,与血清IL-1β、IL-6、IL-8、TNF-α水平呈正相关（P＜0.05）;CTRP-6、CTRP-9水平与FEV₁％、FEV₁/FVC呈正相关,与血清IL-1β、IL-6、IL-8、TNF-α水平呈负相关（P＜0.05）。结论：血清CTRP-4水平升高和CTRP-6、CTRP-9水平降低与老年AECOPD患者肺功能降低和炎症反应有关,可能成为老年AECOPD防治的潜在靶点。     

慢性阻塞性肺疾病患者血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3水平与肺功能及认知功能障碍的关系研究

摘要 目的：探讨慢性阻塞性肺疾病（COPD）患者血清8-异前列腺素F2α（8-iso-PGF2α）、低氧诱导因子（HIF-1α）、中性粒细胞明胶酶相关脂质运载蛋白（NGAL）、半胱氨酸天冬酶-3（caspase-3）水平与肺功能及认知功能障碍的关系。方法：选取2018年3月至2020年6月期间我院收治的62例COPD合并认知功能障碍患者（认知功能障碍组）,另选取50例COPD未合并认知功能障碍患者为对照组。比较两组血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3水平和肺功能、蒙特利尔认知评估量表（MoCA）评分,分析COPD合并认知功能障碍患者血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3与肺功能、MoCA评分的相关性。结果：认知功能障碍组血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3水平高于对照组（P＜0.05）,认知功能障碍组第1秒用力呼气容积（FEV₁）、FEV₁与用力肺活量比值（FEV₁/FVC）、 FEV₁占预计值百分数(FEV₁%pred)、MoCA评分均低于对照组（P＜0.05）。Pearson相关分析结果显示COPD合并认知功能障碍患者血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3水平与FEV₁、FEV₁/FVC、FEV₁%pred、MoCA评分均呈负相关（P＜0.05）。结论：COPD合并认知功能障碍患者血清8-iso-PGF2α、HIF-1α、NGAL、caspase-3水平较COPD未合并认知功能障碍患者明显升高,8-iso-PGF2α、HIF-1α、NGAL、caspase-3升高与肺功能下降和认知功能受损均存在相关性,对COPD患者病情及认知功能障碍具有一定预测价值。     

补肺活血胶囊联合喘可治注射液对慢性阻塞性肺疾病稳定期患者肺功能、 血气指标以及血液流变学的影响

摘要 目的：探讨补肺活血胶囊联合喘可治注射液对慢性阻塞性肺疾病（COPD）稳定期患者肺功能、血气指标以及血液流变学的影响。方法：选取我院于2017年8月到2019年12月期间接收的126例COPD稳定期患者,按照随机数字表法将患者分为对照组（n=63）和研究组（n=63）,对照组给予静注喘可治注射液,研究组在对照组的基础上联合补肺活血胶囊治疗,均治疗12周。比较两组患者疗效、肺功能、血气指标以及血液流变学,记录两组治疗期间不良反应情况。结果：治疗12周后,研究组的临床总有效率84.13%（53/63）高于对照组66.67%（42/63）（P<0.05）。两组第1秒用力呼气容积（FEV₁）、用力肺活量（FVC）、FEV₁/FVC均较治疗前升高,且研究组高于对照组（P<0.05）。两组治疗12周后动脉氧分压（PaO₂）较治疗前升高,且研究组高于对照组（P<0.05）;两组治疗12周后动脉二氧化碳分压（PaCO₂）较治疗前降低,且研究组低于对照组（P<0.05）。两组血浆黏度、纤维蛋白原、全血黏度水平均下降,研究组较对照组低（P<0.05）。两组不良反应发生率比较无差异(P>0.05)。结论：COPD稳定期患者在喘可治注射液的基础上联合补肺活血胶囊治疗,血气指标、肺功能以及血液流变学可得到显著改善,且用药安全性好,疗效较好。     

阿托伐他汀对慢性阻塞性肺疾病合并肺动脉高压患者外周血ROCK2激酶活性及肺动脉压力的影响

目的：探讨口服阿托伐他汀片对慢性阻塞性肺疾病（chronic obstructive pulmonary Disease,COPD）合并肺动脉高压（pul-monary hypertension,PH）患者外周血ROCK2激酶活性及肺动脉压力的影响。方法：选取COPD合并PH患者60例为研究对象,并将其随机分为对照组（给予吸氧、抗感染、化痰、平喘等基础治疗）和阿托伐他汀治疗组（在基础治疗的基础上给予阿托伐他汀片20mg／d治疗）;随访观察周期12周,于试验开始前和结束后检测外周血ROCK2的活性,利用彩色多普勒检测肺动脉压力的变化,肺功能变化（测定FEV1,FVC）。结果：与对照组比较,阿托伐他汀治疗可显著降低患者血浆中ROCK2的水平（P〈0．01）;降低患者的肺动脉压力,改善患者的肺功能（FEV1,FVC）,P均〈0．05。结论：在常规吸氧、抗感染等治疗的基础上,联合应用阿托伐他汀可显著降低ROCK2激酶的活性和肺动脉压力,从而改善肺功能。     

The outcome of pulmonary hypertension and its association with pulmonary artery dilatation

Background

Pulmonary artery (PA) dilatation is often seen in pulmonary hypertension (PH) and is considered a long-term consequence of elevated pressure. The PA dilates over time and therefore may reflect disease severity and duration. Survival is related to the stage of the disease at the time of diagnosis and therefore PA diameter might be used to predict prognosis. This study evaluates the outcome of patients with pulmonary arterial hypertension (PAH) and chronic thrombo-embolic pulmonary hypertension (CTEPH) and investigates whether PA diameter at the time of diagnosis is associated with mortality.

Methods

Patients visiting an outpatient clinic of a tertiary centre between 2004 and 2018 with a cardiac catheterisation confirmed diagnosis of PAH or CTEPH and a CT scan available for PA diameter measurement were included. PA diameter and established predictors of survival were collected (New York Heart Association (NYHA) class, N‑terminal pro-brain natriuretic peptide (NT-proBNP) level and 6‑min walking distance (6MWD)).

Results

In total 217 patients were included (69% female, 71% NYHA class ≥III). During a median follow-up of 50 (22–92) months, 54% of the patients died. Overall survival was 87% at 1 year, 70% at 3 years and 58% at 5 years. The mean PA diameter was 34.2 ± 6.2 mm and was not significantly different among all the diagnosis groups. We found a weak correlation between PA diameter and mean PA pressure ( r = 0.23, p < 0.001). Male sex, higher age, shorter 6MWD and higher NT-proBNP level were independently associated with mortality, but PA diameter was not.

Conclusion

The prognosis of PAH and CTEPH is still poor. Known predictors of survival were confirmed, but PA diameter at diagnosis was not associated with survival in PAH or CTEPH patients.

     

Distribution of the pulmonary artery and vein in the chimpanzee lung

Lungs of two chimpanzees (Pan troglodytes) were examined. The right pulmonary artery runs across the ventral side of the right upper lobe bronchiole and, then across the dorsal side of the right middle lobe bronchiole. Thereafter, it runs between the dorsal bronchiole system and the lateral bronchiole system, along the right bronchus. During its course, it gives off arterial branches which run along each bronchiole. The left pulmonary artery runs across the dorsal side of the left middle lobe bronchiole and then between the dorsal bronchiole system and the lateral bronchiole system. The branches of the pulmonary artery run mainly along the dorsal or lateral side of the bronchiole. The pulmonary veins run mainly along the ventral or medial side of the bronchioles, and between them. Finally, they enter the left atrium with four large veins, i.e. the common trunk of the right upper lobe vein and the right middle lobe vein, right lower lobe pulmonary venous trunk, left middle lobe vein, and left lower lobe pulmonary venous trunk.     

Distribution of the pulmonary artery and vein of the orangutan lung

The distribution of the pulmonary artery and vein of the orangutan lung was examined. The right pulmonary artery runs obliquely across the ventral side of the right bronchus at the caudally to the right upper lobe bronchiole. It then runs across the dorsal side of the right middle lobe bronchiole. Thereafter it runs obliquely across the dorsal side of the right bronchus, and then along the dorso-medial side of the right bronchus. This course is different from that in other mammals. During its course, it gives off branches which run mainly along the dorsal or lateral side of each bronchiole. The left pulmonary artery runs across the dorsal side of the left middle lobe bronchiole, then along the dorso-lateral side of the left bronchus, giving off branches which run along each bronchiole. The pulmonary veins run mainly the ventral or medial side of, along or between the bronchioles. In the left lung, the left middle lobe vein has two trunks; one enters the left atrium, and the other enters the left lower lobe pulmonary venous trunk. This is also different from that found in most mammals. Finally, the pulmonary veins enter the left atrium with four large veins.     

Quadricuspid pulmonary valve and left pulmonary artery aneurysm in an asymptomatic patient assessed by cardiovascular MRI

We present a coincidental finding of quadricuspid pulmonary valve and left pulmonary artery aneurysm. As both the pulmonary valve and the pulmonary trunk with its main branches are hard to visualise with cardiac ultrasound, most abnormalities described so far are from autopsy series. With the increasing use of CMR and its excellent potential for visualising both pulmonary valve and pulmonary arteries, we believe more cases will be discovered in the near future. Although pulmonary artery aneurysm are rare, timely detection may prevent lethal bleeding.     

Distribution of the pulmonary artery and vein in the lung of the crab-eating monkey (Macaca fascicularis)

In the lung of the crab-eating monkey (Macaca fascicularis), the right pulmonary artery runs across the ventral side of the right upper lobe bronchiole and the dorsal side of the right middle lobe bronchiole. Thereafter, it courses along the dorso-lateral side of the right bronchus, between the dorsal and lateral bronchiole systems. During this course, the right pulmonary artery gives off arterial branches running mainly along the dorsal or lateral side of each bronchiole. The left pulmonary artery runs across the dorsal side of the left middle lobe bronchiole, and is then distributed as in the right lower lobe. The pulmonary veins run mainly along the ventral or medial side of the bronchiole in the upper and middle lobes whereas, in the lower lobe, they run ventrally, and between the bronchioles. Finally they enter the left atrium as four large veins.     

Chronic thromboembolic pulmonary hypertension

Chronic pulmonary thromboembolic disease is an important cause of severe pulmonary hypertension, and as such is associated with significant morbidity and mortality. The prognosis of this condition reflects the degree of associated right ventricular dysfunction, with predictable mortality related to the severity of the underlying pulmonary hypertension. Left untreated, the prognosis is poor. Pulmonary endarterectomy is the treatment of choice to relieve pulmonary artery obstruction in patients with chronic thromboembolic pulmonary hypertension and has been remarkably successful. Advances in surgical techniques along with the introduction of pulmonary hypertension-specific medication provide therapeutic options for the majority of patients afflicted with the disease. However, a substantial number of patients are not candidates for pulmonary endarterectomy due to either distal pulmonary vascular obstruction or significant comorbidities. Therefore, careful selection of surgical candidates in expert centres is paramount. The current review focuses on the diagnostic approach to chronic thromboembolic pulmonary hypertension and the available surgical and medical therapeutic options.

Electronic supplementary material

The online version of this article (doi:10.1007/s12471-014-0592-2) contains supplementary material, which is available to authorized users.     

部超声在新生儿呼吸窘迫综合征临床诊断及肺泡表面活性物质治疗效果评估中的应用价值

摘要 目的：研究肺部超声在新生儿呼吸窘迫综合征（NRDS）临床诊断及肺泡表面活性物质（PS）治疗效果评估中的应用价值。方法：将我院于2018年6月～2020年3月期间诊治的80例NRDS患儿纳入研究,记作NRDS组。另取同期80例健康新生儿作为对照组。对所有新生儿进行系统的肺部超声检查并评分,并比较NRDS组和对照组检查结果。将NRDS患儿根据胎龄的不同分成＜30周亚组以及≥30周亚组,比较两组肺部超声检查结果。此外,将所有NRDS患儿按照是否接受PS治疗分成治疗组与非治疗组,比较两组肺部超声评分。结果：NRDS组肺实变、胸膜线异常、支气管充气征、融合B线、肺泡间质综合征、胸腔积液人数占比均高于对照组（均P＜0.05）。胎龄<30周亚组肺泡间质综合征人数占比低于胎龄≥30周亚组患儿,而胸腔积液人数占比高于胎龄≥30周亚组患儿（均P＜0.05）。治疗组治疗后12 h、24 h时的肺部超声评分分别为（15.23±3.15）分、（11.37±2.01）分,均低于非治疗组的（19.45±3.28）分、（16.48±2.83）分（均P＜0.05）。结论：肺部超声作为无创且实时监测手段,诊断NRDS的临床价值较高,且肺部超声评分可作为有效评估NRDS患儿接受PS治疗效果的指标,具有较好的临床应用价值。     

Distribution of the pulmonary artery and vein in the lung of the white handed gibbon

The lungs of four white handed gibbons (Hylobates agilis) were examined. The right pulmonary artery runs across the ventral side of the right upper lobe bronchiole, and then traverses the dorsal side of the right middle lobe bronchiole. Thereafter, it runs along the dorso-lateral side of the right bronchus, between the dorsal bronchiole system and the lateral bronchiole system, and gradually follows the dorsal side of the right bronchus. During its course, it gives off arterial branches which run along each bronchiole. The left pulmonary artery runs across the dorsal side of the left middle lobe bronchiole and then along the left bronchus as in the right lung. The branches of the pulmonary artery run mainly along the dorsal or lateral side of the bronchiole, while the pulmonary veins run mainly the medial side of the bronchioles or between them. However, in a few portions, the pulmonary veins run the lateral side of the bronchioles. Finally, they enter the left atrium with four large veins i.e. the common trunk of the right upper lobe vein and right middle lobe vein, right lower lobe pulmonary venous trunk, left middle lobe vein, and left lower lobe pulmonary venous trunk.     

Pulmonary artery calcification in racehorses may be related to transient and repeated increases in arterial pressure during exercise

Calcification of the pulmonary artery has been found in a large number of racing horses. The majority of calcified lesions are found immediately distal to the primary arterial bifurcation. Increased arterial wall stress levels have been previously demonstrated at these locations, with the wall stress levels increasing under intra-luminal pressures associated with exercise. We hypothesize therefore that the formation of calcified lesions is mediated by transient and repeated increases in pulmonary artery intra-luminal pressure. The presence of calcified lesions would likely further exacerbate the levels of wall stress, leading to growth of the lesions. A level of wall stress may exist above which calcified lesions form, and a second level may exist above which the calcified lesions grow at an increased rate. A computer model of pulmonary artery wall stress with calcified lesions was created, and wall stress levels were found to be greatest at the periphery of the calcified lesions. Osteo/chondrocyte-like cells have also been found at the periphery of the calcified lesions and could be responsible for collagen deposition and lesion growth, mediated by local wall stress levels. These increased levels of wall stress could place racehorses at a greater risk of acute pulmonary arterial rupture at the site of the calcified lesions, due to the high levels of intra-luminal pressure within the pulmonary artery during exercise. The hypothesis may also have implications in the etiology of human vascular diseases.