【摘要】 目的 探讨肺动脉高压患者药物靶向治疗的效果与耐受性。 方法 回顾分析2008年1月〖CD3/5〗2009年8月期间8例肺动脉高压患者分别接受波生坦及西地那非治疗的临床资料,评估其临床表现、WHO肺动脉高压功能分级、6 min步行距离及肺动脉收缩压在基线及治疗3个月后的变化。 结果 治疗后3个月,患者均能耐受药物治疗,无严重不良反应发生。WHO肺动脉高压功能分级在治疗前平均(31±04),治疗后为(23±09),明显得到改善(Plt;005)。肺动脉收缩压在治疗前平均(695±112 ) mm Hg(1 mm Hg=0133 kPa),治疗后为(483±124) mm Hg,明显降低(Plt;005)。6 min步行距离在治疗前平均(324±48) m,治疗后为(400±43) m,明显延长(Plt;005)。 结论 肺动脉高压患者药物靶向治疗的疗效显著,且耐受良好。【Abstract】 Objective To examine the effects of target medical therapy in patients with pulmonary arterial hypertension(PAH). Methods To determine the safety and efficacy of bosentan and sildenafil in eight patients with PAH.The patients’ clinical features, six minutes walking diastance, WHO functional class and systolic pulmonary arterial pressure (SPAP) were measured at baseline and at three months after initiating target medial treatment. Results At the three months followup assessments, WHO functional class was improved with 31±04 vs 23±09 (Plt;005); SPAP was significantly decreased with(695±112 ) mm Hg vs (483±124) mm Hg (Plt;005), the six minutes walking distance was significantly increased with(324±48) m vs(400±43) m (Plt;005). Target medical treatment was well tolerated. Conclusion Target medical treatment is well tolerated and has beneficial effects on PAH.
Abstract: Objective To study the pathophysiological mechanism of the morphological change of immature pulmonary vessels in the piglet model of congenital heart defect with decreased pulmonary blood flow established with balloon atrial septostomy and pulmonary artery banding. Methods Twenty piglets at an age of one to two months were divided into three groups with random number table. For the control group (group C,n=6), small incisions were carried out on the right chest to produce a transient reduction in the pulmonary blood; for the lowmedium pulmonary artery stenosis group (group T1, n=7), the balloon dilator was delivered through the surface of the right atrium and septostomy and pulmonary artery banding were performed, and the systolic transpulmonary artery banding pressure (Trans-PABP) was controlled to be 20.30 mm Hg; For the severe pulmonary artery stenosis group (group T2, n=7), the same surgical procedures with group T1 were performed while TransPABP was controlled to be more [CM(159mm]than 3050 mm Hg.At 2 months after surgery respectively,a lung tissue of 1.0 cm×0.8 cm×0.8 cm from the lateral segment of the right middle lobe was taken out to be observed under optic microscope. The morphological change of the distal arterioles was detected. Furthermore, the content of vascular endothelial growth factor (VEGF) and matrix metalloproteinase2( MMP2) were also examined by the method of enzymelinked immunosorbent assay (ELISA). Results The model was successfully established in all the survival piglets of the group T1 and group T2. Two months after operation, the inner diameter of the pulmonary arterioles in group T1 was significantly higher than that in group C (82.89±10.72 μm vs.74.12±9.28 μm;t=－5.892, Plt;0.05), so as group T2 (85.47±5.25 μm vs.74.12±9.28 μm;t=-6.325, Plt;0.05); the number of arterioles per square centimeter (NAPSC) of group T1 was significantly lower than that of the group C (229.70±88.00 entries/cm 2 vs. 431.50±40.60 entries/cm2; t=39.526, Plt;0.05), so as group T2 (210.00±40.30 entries/cm2 vs. 431.50±40.60 entries/cm2; t=67.858, Plt;0.05). Two months after operation, the lung expression of MMP -2 and VEGF in group T1 was significantly lower than that in group C (58.30±19.60 ng/ml vs. 81.20±16.70 ng/ml, t=14.261, Plt;0.05; 17.80±3.00 pg/ml vs. 21.40±3.80 pg/ml, t=8.482, P＜0.05), so does group T2 (42.10±15.20 ng/ml vs. 81.20±16.70 ng/ml, t=27.318, P＜0.05; 12.30±3.20 pg/ml vs. 21.40±3.80 pg/ml, t=15.139, P＜0.05). Conclusion Structural remodeling of pulmonary extracellular matrix is an important feature of the piglet model of congenital heart defect with decreased pulmonary blood flow. The arterioles show significant hypoplasia or degradation. Change in the structural proteins and cytokines during the reduction of blood in the lung is the key to structural remodeling.
Objective To analyze the clinical characteristics and diagnostic methods of primary pulmonary cryptococcosis. Methods The medical records of adult HIV-negative patients diagnosed with primary pulmonary cryptococcosis between 2006 and March 2011 were reviewed retrospectively. Results 90 patients were enrolled in the study. The mean( ±SD) age was ( 46. 3 ±12. 42) years( range 19 to 71 years) . The clinical manifestations of pulmonary cryptococcosis were mild without obvious physical signs. The imaging features can be classified into 3 types. Nodule or mass type was common. The right lung and lower lobe were most commonly involved. There was no significant difference of the lesion type between the groups with or without underlying diseases ( P gt;0. 05) . Sputum or BALF culture for Cryptococcus neoformans yield no positive result. The main diagnostic methods were video-assisted thoracic surgery( VATS, 42 cases) , transbronchial lung biopsy( TBLB, 28 cases) and transthoracic needle aspiration biopsy( TNAB, 14 cases) . The latex agglutination( LA) test yield positive results in 31 patients out of 48 patients( 64. 58% ) . The LA test positive group often used TBLB as diagnostic method( 64. 52% ) .Meanwhile the LA test negative group and the group without LA test often used thoracoscope as diagnostic method( 47. 06% and 76. 19% ) . There was significant difference in diagnostic method between the three groups( P lt;0. 05) . Conclusions It is not impossible to acquire pulmonary cryptococcosis in immunocompetent patients. The clinical manifestations and imaging features of pulmonary cryptococcosis were lack of characteristics. The diagnosis level can be improved by invasive examination such as TBLB and TNAB. The LA test for Cryptococcus neoformans can be used as an early noninvasive diagnostic method.
ObjectiveTo investigate the clinical characteristics of non-tuberculous mycobacterium (NTM) pulmonary disease and pulmonary tuberculosis, as well as the bacterial distribution of NTM pulmonary disease. Methods The bacterial distribution and clinical characteristics of 104 patients with NTM lung disease hospitalized in Jiangxi Provincial People’s Hospital from May 2017 to May 2020 were retrospectively analyzed, as well as the clinicplal characteristics of 155 patients with tuberculosis hospitalized during the same period. Results The age of NTM lung disease group [(60±15) years] was higher than that of tuberculosis group [(55±19) years]. There were statistically significant differences in basic diseases (such as malignant tumor, type 2 diabetes, old tuberculosis, bronchiectasis), laboratory examination (such as blood routine examination, albumin) and chest imaging characteristics between the two groups (P<0.05). There was no significant difference in clinical symptoms (such as cough, sputum or fever) (P>0.05). The common underlying diseases of NTM lung disease were malignant tumor (29%), bronchiectasis (21%), chronic obstructive pulmonary disease (19%), etc. The common clinical symptoms of NTM lung disease included cough, sputum, fever, hemoptysis, chest tightness and shortness of breath, and other non-specific respiratory symptoms. The common manifestations of NTM lung disease on chest high-resolution CT (HRCT) included patchy images (82%), mediastinal lymph node enalargement (35%), pleural thickening (31%), pleural effusion (26%) and other signs. The isolates of NTM included Mycobacterium avium (50%), Mycobacterium intracellulare (21%), Mycobacterium chelonae/abscessus (14%), Mycobacterium fortuitum (5%), Mycobacterium gordonae (4%), Mycobacterium gilvum (3%), and Mycobacterium smegmatis (3%). Multivariate Logistic regression analysis showed that advanced age (OR=1.027) was a risk factor for NTM lung disease. Conclusions The clinical manifestations of NTM lung disease and tuberculosis are similar and difficult to distinguish. For male patients over 60 years old with malignant tumor, old tuberculosis, bronchiectasis and other basic diseases, and the chest HRCT findings are mainly bronchiectasis, NTM lung disease should be actively excluded. There is little difference in clinical manifestations between different strains of NTM lung disease, and the treatment cycle of NTM lung disease is long and easy to be interrupted, requiring enhanced follow-up.
Objective To evaluate the efficacy and safety of whole lung lavage in the treatment of pulmonary alveolar proteinosis ( PAP) .Methods Twelve patients who were diagnosed as PAP from September 2008 to October 2011 in Hunan Occupational Disease Hospital were recruited in the study. The changes of dyspnea symptom, lung-function, arterial blood gas, and chest image were compared before and after whole lung lavage treatment. Meanwhile, the safety of lung lavage was evaluated. Results All patients were relieved from dyspnea. The lung function, hypoxia, hyperventilation, and chest image were all obviously improved. The vital signs in the process of lung lavage were stable without serious complications. Conclusion Whole lung lavage is an effective and safe treatment for PAP.
Objective To develop an innovative recognition algorithm that aids physicians in the identification of pulmonary nodules. MethodsPatients with pulmonary nodules who underwent thoracoscopic surgery at the Department of Thoracic Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School in December 2023, were enrolled in the study. Chest surface exploration data were collected at a rate of 60 frames per second and a resolution of 1 920×1 080. Frame images were saved at regular intervals for subsequent block processing. An algorithm database for lung nodule recognition was developed using the collected data. ResultsA total of 16 patients were enrolled, including 9 males and 7 females, with an average age of (54.9±14.9) years. In the optimized multi-topology convolutional network model, the test results demonstrated an accuracy rate of 94.39% for recognition tasks. Furthermore, the integration of micro-variation amplification technology into the convolutional network model enhanced the accuracy of lung nodule identification to 96.90%. A comprehensive evaluation of the performance of these two models yielded an overall recognition accuracy of 95.59%. Based on these findings, we conclude that the proposed network model is well-suited for the task of lung nodule recognition, with the convolutional network incorporating micro-variation amplification technology exhibiting superior accuracy. Conclusion Compared to traditional methods, our proposed technique significantly enhances the accuracy of lung nodule identification and localization, aiding surgeons in locating lung nodules during thoracoscopic surgery.
Objective To investigate the relationship of pulmonary surfactant protein D( SP-D) with chronic obstructive pulmonary disease ( COPD) by measuring SP-D level in serum and lung tissue of rats with COPD.Methods The rat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide ( LPS) . Thirty male SD rats were randomly divided into a control group, a LPS group, and a COPD group( n =10 in each group) . The pathologic changes of lung tissue and airway were observed under light microscope by HE staining. Emphysema changes were evaluated by mean linear intercept ( MLI) of lung and mean alveolar number ( MAN) . The level of SP-D in serum was measured by enzymelinked immunosorbent assay ( ELISA) . The expression of SP-D in lung tissue was detected by Western-blot and immunohistochemistry.Results The MLI obviously increased, and MAN obviously decreased in the COPD group compared with the control group ( Plt;0.05) . There was no significant difference in the MLI and MAN between the LPS group and the control group ( Pgt;0.05) . The serum SP-D level was ( 49.59 ±2.81) ng/mL and ( 53.21±4.17) ng/mL in the LPS group and the COPD group, which was significantly higher than that in the control group [ ( 42.14±2.52) ng/mL] ( Plt;0.05) . The expression of SP-D in lung tissue was 0.56±0.01 and 0.63±0.01 in the LPS group and the COPD group, which was also obviously ber than that in the control group ( 0.39 ±0.01) ( Plt;0.05) .Meanwhile the SP-D levels in serumand lung tissue were higher in the COPD group than those in the LPS group ( Plt;0.05) . The levels of SP-D between serum and lung tissue were positively correlated in all three groups ( r=0.93, 0.94 and 0.93, respectively, Plt;0.01) .Conclusion Both the SP-D level in serum and in lung tissue increase significantly in COPD rats and correlate well each other, which suggests that SP-D may serve as a biomarker of COPD.
Objective To investigate the incidence and management of CTEPH in the Department of Pulmonary and Critical Care Medicine in Xijing Hospital to enrich the epidemiological data of chronic thromboembolic pulmonary hypertension (CTEPH) in China.Methods We conducted a retrospective study to investigate the incidence and management of CTEPH in the Department of Pulmonary and Critical Care Medicine in Xijing Hospital from 2008 to 2012. Results The incidence of CTEPH was 5.24% . About 62.90% of venous thromboembolism/pulmonary embolism (VTE/PE) patients were unprovoked, and about 53.85% of CTEPH patients was unprovoked. About 38% of CTEPH patients had no history of VTE, and 62% of CTEPH patients had no history of acute pulmonary embolism. None of the CTEPH patients was treated by pulmonary thromboendarterctom (PTE) , and about 53.85% of patients were only given anticoagulant monotherapy. Conclusions The incidence of CTEPH is higher in our hospital than reported. This phenomenon may be related to the lack of awareness of risk factors of CTEPH and the insufficient thrombolytic and anticoagulant therapy to acute pulmonary embolism. It’s very urgent to standardize the diagnosis and management of CTEPH in pulmonologists.
The body of patient undergoing cardiopulmonary resuscitation after cardiac arrest experiences a process of ischemia, hypoxia, and reperfusion injury. This state of intense stress response is accompanied with hemodynamic instability, systemic hypoperfusion, and subsequent multiple organ dysfunction, and is life-threatening. Pulmonary vascular endothelial injury after cardiopulmonary resuscitation is a pathological manifestation of lung injury in multiple organ injury. Possible mechanisms include inflammatory response, neutrophil infiltration, microcirculatory disorder, tissue oxygen uptake and utilization disorder, etc. Neutrophils can directly damage or indirectly damage lung vascular endothelial cells through activation and migration activities. They also activate the body to produce large amounts of oxygen free radicals and release a series of damaging cytokines that further impaire the lung tissue.
ObjectiveTo observe the pathological changes in heart and lung tissues in rats with pulmonary hypertension induced by monocrotaline. MethodsTwenty-four male Sprague-Dawley rats were randomly and equally divided into an experimental group and a control group. The rats in the experimental group were intraperitoneally injected with monocrotaline to induce pulmonary hypertension, and the rats in the control group were treated with saline. All rats were fed for 3 weeks, and the general situation were observed. Then the rats were sacrificed for measurement of mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index [RV/(LV+S)], changes of myocardial cells and lung vascular, calculated density of middle membrane smooth muscle cells (SMC) in medium/small pulmonary arteries accompanied with bronchi and alveoli, media thickness of pulmonary artery (PAMT), the percentage of wall thickness with outer diameter (WT%), the percentage of wall area with total area (WA%), the average diameter of myocardial cells (AD), and myocardial nuclei density (MND). ResultsCompared with the control group, the condition of rats in the experimental group were getting worse obviously.mPAP and RV/(LV+S) were both increased (both P < 0.05). The observation by light microscope revealed that obvious myocardial hypertrophy and structure disturbances, severe luminal stenosis of medium/small pulmonary arteries, medial thickening, infiltration of inflammatory cell in tissue space, proliferation of unorganized collagen fibers in the experimental group. The observation by electronic microscope showed proliferation of endothelial cell with irregular nuclei, increased organelles and vacuoles in the experimental group. The differences in SMC, PAMT, WT%, WA%, AD, and MND were significant between two groups (all P < 0.05). ConclusionsThe monocrotaline can induced pulmonary hypertension and right ventricular hypertrophy. The mechanism may be related to severe stenosis or occlusion of the vessel lumen caused by plexiform proliferation of endothelial cells, proliferation of smooth muscle cells and collagen fibers, compensatory hypertrophy and hyperplasia of myocardial cells.