Pharmacological characterization of the late phase reduction in lung functions and correlations with microvascular leakage and lung edema in allergen-challenged Brown Norway rats

Late phase airflow obstruction and reduction in forced vital capacity are characteristic features of human asthma. Airway microvascular leakage and lung edema are also present in the inflammatory phase of asthma, but the impact of this vascular response on lung functions has not been precisely defined. This study was designed to evaluate the role of increased lung microvascular leakage and edema on the late phase changes in forced vital capacity (FVC) and peak expiratory flow (PEF) in allergen-challenged Brown Norway rats using pharmacological inhibitors of the allergic inflammatory response. Rats were sensitized and challenged with ovalbumin aerosol and forced expiratory lung functions (FVC, PEF) and wet and dry lung weights were measured 48 h after antigen challenge. Ovalbumin challenge reduced FVC (63% reduction) and PEF (33% reduction) and increased wet (65% increase) and dry (51% increase) lung weights. The antigen-induced reduction in FVC and PEF was completely inhibited by oral treatment with betamethasone and partially attenuated by inhibitors of arachidonic acid metabolism including indomethacin (cyclooxygenase inhibitor), 7-TM and MK-7246 (CRTH2 antagonists) and montelukast (CysLT₁ receptor antagonist). Antagonists of histamine H₁ receptors (mepyramine) and 5-HT receptors (methysergide) had no significant effects indicating that these pre-formed mast cell mediators were not involved. There was a highly significant (P < 0.005) correlation for the inhibition of FVC reduction and increase in wet and dry lung weights by these pharmacological agents. These results strongly support the hypothesis that lung microvascular leakage and the associated lung edema contribute to the reduction in forced expiratory lung functions in antigen-challenged Brown Norway rats and identify an important role for the cyclooxygenase and lipoxygenase products of arachidonic acid metabolism in these responses.     

Pulmonary embolism,part II: Management

Acute pulmonary embolism (PE) bears a significant burden on health and survival. Rapid and accurate risk stratification and management are of paramount importance to ensure the highest quality of care. This present article summarizes currently available and emerging management strategies for the disease. The authors not only review current evidence regarding early therapy of acute PE, including supportive care, anticoagulation, thrombolysis, surgical and catheter-based treatment, but also the possible role of mechanical circulatory support in PE. The authors also discuss complications related to PE and its management.     

Protein Concentration and Hydrostatic Pressure in Subcutaneous Tissue of Rats in Hypoproteinemia

Protein concentration and hydrostatic pressure were measured in subcutaneous tissue of rats during development of aminonucleoside nephrosis. Samples of interstitial fluid for protein analysis were collected from subcutaneous tissue by a wick method, and hydrostatic pressure was measured by a modified Scholander technique. When the serum protein concentration was reduced from 6.1 to 4.8 g/100 ml, interstitial fluid protein concentration fell from 3.0 to 1.1 g/100 ml. This corresponds to a reduction of calculated oncotic pressures from 18.0 to 13.0 mm Hg and from 7.8 to 3.0 mm Hg in serum and interstitial fluid, respectively, thus leaving a nearly constant net transcapillary oncotic pressure. When serum protein concentration was further reduced to 3.8 g/100 ml, interstitial fluid protein concentration was reduced to 0.5 g/100 ml, reducing net transcapillary oncotic pressure by 2–3 mm Hg. The average hydrostatic pressure in subcutis was 1.0 mm Hg sub-atmospheric under control conditions and did not change during hypoproteinemia. The results indicate that a reduction of interstitial protein concentration is an important factor in preventing edema formation in hypoproteinemia.     

不同CT窗技术及后处理技术对肺栓塞的诊断价值

目的评价不同CT窗技术及后处理技术对肺栓塞的诊断价值。方法回顾性分析2018年9月～2020年1月在我院行CTPA确诊的45例肺栓塞患者的资料,分别应用常规纵膈窗及常用调节窗、常规纵膈窗+调节窗观察肺栓塞的位置(段以上、段及段以下)及阳性血管数,以纵膈窗联合调节窗检出的肺栓塞作为金标准。比较最大密度投影(MIP)、多平面重组(MPR)和容积重建(VR)三种后处理技术对不同位置的肺动脉显示率,组间比较采用χ~2检验。结果段及段以下肺栓塞,单独使用调节窗的漏诊率低于单独使用纵膈窗,分别为3.3%、12.5%,差异有统计学意义(P0.05)。段以上肺栓塞,单独应用常用调节窗、纵膈窗漏诊率分别为4.5%、13.6%,组间比较差异无统计学意义(P0.05)。MPR对段及段以下肺动脉栓塞的显示率优于MIP及VR影像,差异具有统计学意义(P0.05)。结论在阅读CTPA图像中,单纯使用常规纵膈窗或常用调节窗都可漏掉部分栓塞,特别是较小血管的栓塞,临床工作中,应常规使用纵膈窗+常用调节窗宽、MPR重建技术减少肺栓塞的漏诊。     

SOX5基因多态性与慢性阻塞性肺疾病及并发症肺动脉高压的关联性分析

目的:通过观察慢性阻塞性肺疾病(COPD)稳定期患者、COPD合并肺动脉高压(PH)患者及健康者之间SOX5基因单核苷酸多态性(SNPs)的分布差异,初步探索SOX5基因多态性与COPD相关PH易感性的关联。方法:连续选择2013年4月~2015年4月就诊于宁夏人民医院总院及宁南分院呼吸内科的COPD稳定期患者250例,根据COPD诊治指南(2013年版)诊断标准入组,并且就诊当天全部进行超声心动图检查,根据肺动脉收缩压(PASP)结果分为COPD合并PH组(PASP≥50 mm Hg)103例和COPD非PH组(PASP50 mm Hg)147例。健康对照组选择同期在宁夏人民医院体检的健康者127例。使用Sequenom Mass ARRAY SNP检测系统检测所有受试者SOX5基因rs10842262和rs11046966位点的基因型,统计基因型频率并对比各组间差异。结果:健康对照组与COPD组之间(包括COPD合并PH及未合并PH组的全部患者)以及COPD合并PH组与COPD非PH组之间在年龄、性别和吸烟指数上的差别均无统计学显著性。健康对照组与COPD组之间SOX5基因rs10842262位点及rs11046966位点基因型频率分布的差异均存在统计学显著性(P0.05)。COPD合并PH组与COPD非PH组之间SOX5基因rs10842262位点及rs11046966位点各基因型频率分布的差异无统计学显著性。结论:SOX5基因rs10842262和rs11046966位点的基因多态性与COPD的易感性相关,但与COPD相关PH的易感性还不能认为有关联。     

肺泡微石症的影像学诊断

目的：探讨肺泡微石症的影像学特征。方法;报道肺泡微石症6例,全部病例均行胸部X线检查,2例行常规CT,1例行HRCT。并对全部影像学表现进行了回顾性分析。结果：6例胸片表现为弥漫粟粒样微细结节（2例）。“鱼子样”或“暴风沙样”（2例）、“白肺样”（1例）及高密度“面纱样”改变（1例）,CT可明确肺内微细结节的钙化密度,肺尖部气肿样改变及支气管血管束增粗并呈钙化密度,HRCT则可进一步显示肺野磨砂玻璃样改变,小叶间隔,叶间胸膜及支气管血管束钙化密度与串珠状增厚,小叶中心分布的微细结节与胸膜下蜂窝,结论：肺泡微石症是一种罕见病,其影像学表现具有特征性,影像学检查尤以HRCT检查对该病的诊断有决定性作用。     

Cellular and humoral mediators of pulmonary edema

Pulmonary edema results from increases in pulmonary capillary hydrostatic pressure and microvascular protein permeability. Mediators that induce pulmonary edema can be subdivided into two classes: (1) mediators that alter pulmonary hydrostatic pressure such as serotonin and (2) mediators that increase capillary permeability and result in increased transport of protein. A recognized important permeability increasing factor in the pulmonary microcirculation is the process of neutrophil activation and concomitant mediator release subsequent to neutrophil sequestration. Increased pulmonary capillary pressure occurring concomitantly with increased permeability greatly enhances protein flux and extravascular fluid accumulation. The rise in capillary hydrostatic pressure is determined by precapillary and postcapillary vessel resistances. Recent data indicate that pulmonary veins are not inert conduits but possess active smooth muscle components which respond to vasoactive agents such as histamine and arachidonic acid metabolites through venoconstriction. It appears that few humoral factors acting independently actually increase pulmonary capillary permeability. In comparison to the systemic microcirculation, the lung microcirculation appears to be more resistant to agents such as histamine and bradykinin which are known permeability-increasing agents in systemic microvessels. This may be important teleologically as the pulmonary microcirculation receives the entire cardiac output.