Adjacent Pulmonary Artery Research Articles

Single-center 10-year retrospective analysis of Amplatzer Vascular Plug 4 embolization for pulmonary arteriovenous malformations with feeding arteries of

To evaluate the efficacy and safety of Amplatzer Vascular Plug 4 (AVP4) embolization in pulmonary arteriovenous malformations (PAVMs) with small- to medium-sized feeding arteries (<6 mm) and to identify factors affecting persistence and the main persistence patterns after embolization. Between June 2013 and February 2023, we retrospectively reviewed 100 patients with 217 treated PAVMs. We included PAVMs with feeding arteries <6 mm, treated with AVP4 embolization, and followed adequately with computed tomography (CT). Technical success was defined as flow cessation observed on angiography. Persistence was defined as less than a 70% reduction of the venous sac on CT. We evaluated adverse events for each embolization session. Patterns of persistence were assessed using follow-up angiography. Univariate and multivariate analyses were performed to evaluate factors affecting persistence based on the 70% CT criteria. Fifty-one patients (48 women, 3 men; mean age: 50.8 years; age range: 16-71 years) with 103 PAVMs met the inclusion criteria. The technical success rate was 100%. The persistence rate was 9.7% (10/103), and the overall adverse event rate was 2.9% (3/103) during a mean follow-up of 556 days (range: 181-3,542 days). In two cases, the persistence pattern confirmed by follow-up angiography involved reperfusion via adjacent pulmonary artery collaterals. The location of embolization relative to the last normal branch of the pulmonary artery was the only factor substantially affecting persistence. Embolization with AVP4 appears to be safe and effective for small- to medium-sized PAVMs. The location of the embolization relative to the last normal branch of the pulmonary artery was found to be the main determinant of persistence. Given the increasing demand for the treatment of small PAVMs, AVP4 embolization could be considered a viable and effective option for managing PAVMs with feeding arteries <6 mm.

BRONCHIECTASIS: MICROBIOME AND INFECTIONS

Due to the degradation of the muscles and elastic connective tissues, bronchiectasis is characterized by a chronic enlargement of the bronchi and bronchioles. The condition is characterized by an ongoing cough, the production of sputum, and infections and can strike at any age. Bronchiectasis may have been less frequent in the 20th century, but it still ranks third among the chronic inflammatory disorders of the airways, behind chronic obstructive pulmonary disease and asthma. Pseudomonas aeruginosa and Haemophilus influenzae are the most frequent bacteria detected in bronchiectasis airways worldwide, but proportions differ amongst bacterial communities. Additionally, Streptococcus, Prevotella, Veillonella, and Staphylococcus have been found in bronchiectasis patients' airways. The symptoms of bronchiectasis, which include worsened sputum production with more blood and purulent discharge, wheezing and dyspnea, as well as fever, are considered to be brought on by bacterial infection. On thin-section CT scans, morphologic criteria include the presence of bronchi within 1 cm of the pleural surface and bronchial dilatation in relation to the adjacent pulmonary artery (signet ring sign). The basic objectives of bronchiectasis care are to preserve adequate lung function, regulate symptoms and enhance patient quality of life while preventing and reducing exacerbations.

Anatomical correlation between left atrium pulmonary vein ablation targets of atrial fibrillation and adjacent bronchi and pulmonary arteries by MSCT

BackgroundThe ablation targets of atrial fibrillation (AF) are adjacent to bronchi and pulmonary arteries (PAs). We used computed tomography (CT) to evaluate the anatomical correlation between left atrium (LA)-pulmonary vein (PV) and adjacent structures.MethodsData were collected from 126 consecutive patients using coronary artery CT angiography. The LA roof was divided into three layers and nine points. The minimal spatial distances from the nine points and four PV orifices to the adjacent bronchi and PAs were measured. The distances from the PV orifices to the nearest contact points of the PVs, bronchi, and PAs were measured.ResultsThe anterior points of the LA roof were farther to the bronchi than the middle or posterior points. The distances from the nine points to the PAs were shorter than those to the bronchi (5.19 ± 3.33 mm vs 8.62 ± 3.07 mm; P < .001). The bilateral superior PV orifices, especially the right superior PV orifices were closer to the PAs than the inferior PV orifices (left superior PV: 7.59 ± 4.14 mm; right superior PV: 4.43 ± 2.51 mm; left inferior PV: 24.74 ± 5.26 mm; right inferior PV: 22.33 ± 4.75 mm) (P < .001).ConclusionsThe right superior PV orifices were closer to the bronchi and PAs than other PV orifices. The ablation at the mid-posterior LA roof had a higher possibility to damage bronchi. CT is a feasible method to assess the anatomical adjacency in vivo, which might provide guidance for AF ablation.

Venous-phase chest CT with reduced contrast medium dose: Utilization of spectral low keV monoenergetic images improves image quality

PurposeIntravenous contrast administration is crucial in many CT examinations but also poses a potential risk to the patient. Monoenergetic images (MonoE) of dual-energy CT systems can virtually increase iodine attenuation and might improve image quality (IQ) if contrast dose is reduced. In this study, we investigated the influence of MonoE on lymph node (LN) delineation and IQ in chest CT examinations with significantly reduced contrast dose (50 %) of a novel dual-layer CT (DLCT). Method30 patients with clinically indicated reduced contrast dose underwent venous-phase chest DLCT scans. Conventional polyenergetic (PolyE) and MonoE images at 40 keV were calculated. The contrast difference of hilar lymph nodes (LN-CD) to the adjacent right pulmonary artery, their signal-to-noise (SNR) and contrast-to-noise-ratio (CNR) were determined. Subjective IQ was evaluated by 2 readers with respect to LN delineation and overall contrast enhancement (CE) using a 5-point-Likert-scale. ResultsLN-CD, SNR and CNR were significantly higher in MonoE than in PolyE images (LN-CD 92.3 ± 37.9 vs. 33.1 ± 14.5 HU, SNR 8.4 ± 3.4 vs. 4.0 ± 1.2, CNR 9.2 ± 6.3 vs. 2.6 ± 1.5; all p < 0.01). The LN delineation (3.7 ± 0.9 vs.1.8 ± 0.7; p < 0.01) and the CE (3.9 ± 0.7 vs. 2.3 ± 0.7; p < 0.01) were rated significantly better for MonoE than for PolyE images. There was no MonoE examination classified as non-diagnostic. ConclusionsSubjective and objective IQ parameters can be significantly improved for venous-phase chest CT examinations with reduced contrast doses by utilization of low-keV MonoE reconstructions. All MonoE images provided sufficient overall CE and therefore reduced contrast doses might be considered in a wider range of DLCT examinations and patients.

Bronchoarterial ratio in never-smokers adults: Implications for bronchial dilation definition.

Bronchiectasis manifests as recurrent respiratory infections and reduced lung function. Airway dilation, which is measured as the ratio of the diameters of the bronchial lumen (B) and adjacent pulmonary artery (A), is a defining radiological feature of bronchiectasis. A challenge to equating the bronchoarterial (BA) ratio to disease severity is that the diameters of airway and vessel in health are not established. We sought to explore the variability of BA ratio in never-smokers without pulmonary disease and its associations with lung function. Objective measurements of the BA ratio on volumetric computed tomography (CT) scans and pulmonary function data were collected in 106 never-smokers. The BA ratio was measured in the right upper lobe apical bronchus (RB1) and the right lower lobe basal posterior bronchus. The association between the BA ratio and forced expiratory volume in 1 s (FEV1 ) was assessed using regression analysis. The BA ratio was 0.79 ± 0.16 and was smaller in more peripheral RB1 bronchi (P < 0.0001). The BA ratio was >1, a typical threshold for bronchiectasis, in 10 (8.5%) subjects. Subjects with a BA ratio >1 versus ≤1 had smaller artery diameters (P < 0.0001) but not significantly larger bronchial lumens. After adjusting for age, gender, race and height, the BA ratio was directly related to FEV1 (P = 0.0007). In never-smokers, the BA ratio varies by airway generation and is associated with lung function. A BA ratio >1 is driven by small arteries. Using artery diameter as reference to define bronchial dilation seems inappropriate.

The relationships of the pulmonary arteries to lung lesions aid in differential diagnosis using computed tomography.

The improvement of the resolution of rapid scanning in multidetector computed tomography (CT) has an increased accuracy that allows for the demonstration of the relationship of the pulmonary arteries and lung lesions, even in the peripheral lung. The purpose of this study is to evaluate the relationship between the pulmonary arteries and lung lesions by CT, and to use this relationship to distinguish between benign and malignant lung lesions. The relationships of the lung lesions and the adjacent pulmonary artery were recorded as encasement, displacement, penetration, in the margin, and disconnection. Statistical analyses were then performed to evaluate the relationship of the pulmonary arteries to each lesion with a focus toward the possibility of malignancy and the degree of pulmonary arterial encasement in the lesion. The relationship between the pulmonary arteries and lung lesions had a statistically significant difference between benignancy and malignancy (P < 0.001). Inter-observer agreement was substantial (κ = 0.639; 95% CI: 0.518-0.719). The average degrees of pulmonary arterial encasement in benign and malignant lesions were 52.1% ± 27.3% and 71.8% ± 18.8%, respectively (P = 0.011). The ROC curve showed that the degree of pulmonary arterial encasement had a moderate discriminating ability in diagnosing lung carcinoma, and the area under the curve was 0.738. The best cutoff value was 44.4%. The relationships of the pulmonary arteries to lung lesions and the degree of pulmonary arterial encasement could be used in differentiating benignancy from malignancy not only for central lung lesions but also peripheral lung lesions.

Bronchiectasis: Mechanisms and Imaging Clues of Associated Common and Uncommon Diseases

Bronchiectasis is permanent irreversible dilatation of the airways and occurs in a variety of pathologic processes. Recurrent infection and inflammation and the resulting chemical and cellular cascade lead to permanent architectural changes in the airways. Bronchiectasis can confer substantial potential morbidity, usually secondary to recurrent infection. In severe cases of bronchiectasis, massive hemoptysis can lead to death. Thin-section computed tomography is the most sensitive imaging modality for the detection of bronchiectasis; findings include bronchial diameter exceeding that of the adjacent pulmonary artery and lack of normal tapering of terminal bronchioles as they course toward the lung periphery. The authors will review various causes of bronchiectasis, including common causes, such as recurrent infection or aspiration, and uncommon causes, such as congenital immunodeficiencies and disorders of cartilage development. The authors will also present an approach emphasizing the distribution (apical versus basal and central versus peripheral) and concomitant findings, such as nodules, cavities, and/or lymphadenopathy, that can assist in narrowing the differential diagnosis. Although an adequate understanding of these underlying causes in conjunction with their specific imaging appearances will allow radiologists to more confidently determine the process causing this common radiologic finding, clinical history and patient demographic characteristics play an integral role in determining a pertinent and concise differential diagnosis.

Accuracy of a computed tomography bronchial wall thickness to pulmonary artery diameter ratio for assessing bronchial wall thickening in dogs.

Computed tomography is increasingly being used in veterinary medicine to evaluate animals with pulmonary signs such as coughing, tachypnea, and exercise intolerance, however, a quantitative measure of bronchial wall thickening has yet to be validated in veterinary medicine. Canine chronic bronchitis is a disease that is characterized histologically by thickening of the bronchial walls. Thoracic CT images of 16 dogs with chronic bronchitis and 72 dogs presenting for conditions unrelated to cough were evaluated. A ratio comparing the bronchial wall thickness to the adjacent pulmonary artery diameter was obtained in the right and left cranial and caudal lung lobes. There was no significant difference in dogs with chronic bronchitis or unaffected dogs between the left and right hemithorax, patient weight, patient age, image slice thickness, or CT machine used. Dogs with chronic bronchitis were found to have a significantly greater ratio than unaffected dogs (P < 0.001). The ratios in the cranial lung lobes were found to be significantly greater than the caudal lung lobes in both chronic bronchitis and unaffected dogs (P < 0.001). A receiver operating characteristic curve of the ratios in the cranial lung lobes had an area under the curve of 0.912, indicating high accuracy in predicting for bronchial wall thickening. A ratio of ≥ 0.6 in the cranial lung lobes was found to have a sensitivity of 77% and specificity of 100% in predicting for the presence of chronic bronchitis, and we propose using this cut-off as supportive of bronchial wall thickening on CT.

Treatment of pulmonary hypertension

The therapeutic approach to the management of pulmonary hypertension (PH) is based on strategies to decrease pulmonary vascular resistance (PVR) whilst ensuring optimal cardiorespiratory support to improve oxygenation. The goal is to maintain appropriate systemic blood pressure, ensure oxygen release to tissues and minimize lesions induced by oxygen and ventilation. Inhaled nitric oxide (iNO) remains the mainstay of treatment for this condition. As an inhaled agent it reaches the alveolar space and diffuses into the vascular smooth muscle of the adjacent pulmonary arteries where it causes vasodilation by increasing guanosine monophosphate (cGMP) levels without affecting systemic vascular tone. Although iNO significantly reduces the need for extracorporeal membrane oxygenation, almost 25-40% of iNO-treated infants are considered iNO non–responders. A complementary vasodilatory pathway in the lung is mediated by cyclic adenosine monophosphate (cAMP); prostacyclin stimulates adenylyl cyclase in vascular smooth muscle cells and causes an increase in intracellular cAMP and vasodilation of the systemic and pulmonary circulatory systems. If given as an inhaled drug the vasodilatory effects of prostacyclin tend to be limited to the pulmonary circulation, making this strategy appealing when acute pulmonary vasodilation is needed. [1] Inhibition of the cGMP-degrading phosphodiesterase (PDE5) and inhibition of the cAMP-degrading phosphodiesterase (PDE3) are two other promising therapies. Sildenafil is a PDE5 inhibitor, the predominant PDE isoform in the lung responsible for the breakdown of cGMP. It acts by enhancing NO-mediated vasodilation and may facilitate iNO discontinuation in infants with critical illness.[2] Milrinone is a PDE3 inhibitor with inotropic and vasodilatory effects; it improves the left ventricular cardiac function both directly and by reducing systemic afterload and exerts also important effects on the pulmonary vasculature by reducing PVR. It may be a plausible agent for treating patients with PH and impaired myocardial function. [3] One of the most potent vasoconstrictors described in the pulmonary vasculature is Endothelin-1 (ET-1). Inhibition of ET-1 mediated vasoconstriction could be achieved by administration of an endothelin receptor antagonist (Bosentan). Bosentan lowers pulmonary artery pressure and PVR in children with diverse causes of PH and may improve oxygenation in neonates with persistent pulmonary hypertension; it has also been successfully used as an adjunctive treatment for children receiving long-term prostacyclin therapy.

Multi-slice computed tomography assessment of bronchial compression with absent pulmonary valve

BackgroundAbsent pulmonary valve is a rare cardiovascular anomaly that can result in profound tracheobronchial compression.ObjectiveTo demonstrate the advantage of multi-slice CT in diagnosing tracheobronchial compression, its severity as related to the adjacent dilated pulmonary arteries, and associated lung and cardiac lesions.Materials and methodsWe included children with absent pulmonary valve who were reviewed by multi-slice CT during a 17-year period. The number and locations of stenoses and lung lesions were noted and the severity of stenosis was categorized. The diameter of the pulmonary artery was measured and associated cardiac defects were demonstrated.ResultsThirty-one children (14 girls and 17 boys) were included. Of these, 29 had ventricular septal defect and 2 had an intact ventricular septum. Twenty-nine children (94%) had tracheobronchial compression, judged to be mild in nine children (31%), moderate in 10 (34%) and severe in 10 (34%). The different locations of the stenosis (carina, main bronchi, lobar and segmental bronchi) were observed. And the number and location of lung lesions demonstrated that the right middle and left upper and lower lobes were often affected. The diameter of the pulmonary artery in these children was well above normal published values, and Spearman rank correlation analysis showed a correlation between the size of the pulmonary artery and the severity of the tracheobronchial stenosis. Nineteen children (61%) underwent surgery and 4 of these children had a multi-slice CT post-operative follow-up study.ConclusionAbsent pulmonary valve can cause significant morbidity and mortality in children. Multi-slice CT can accurately depict areas of tracheobronchial compression, associated lung lesions and cardiac defects, helping to direct the surgeon.

Treated Pulmonary Arteriovenous Malformations: Patterns of Persistence and Associated Retreatment Success

To determine the relative frequencies of persistence patterns in treated pulmonary arteriovenous malformations (PAVMs) and to assess whether there is a difference in retreatment outcomes between PAVMs persisting via recanalization and those persisting via reperfusion. Between May 2003 and May 2011, 23 patients (10 male, 13 female; mean age, 44 years ± 18 [standard deviation]; age range, 12-72 years) who had PAVM embolization, persistence by computed tomography (CT), and a follow-up pulmonary arteriogram were included. This retrospective study was approved by the institutional review board and was fully HIPAA compliant. PAVMs were categorized as having recanalization, defined as persistence maintained by flow through a previously placed coil nest; reperfusion, defined as persistence through small feeders from adjacent normal pulmonary arteries; or incomplete treatment. Fifty-three persistent PAVMs were characterized; 38 of which had postretreatment CT data (median follow-up, 1 year). The retreatment success rate, defined by sac shrinkage on CT images, was assessed. Recanalization was the most common pattern, occurring in 91% (n = 48) of 53 PAVMs. Pulmonary-to-pulmonary reperfusion occurred in 24% (n = 13) of 53 PAVMs. Angioarchitecture, coil-sac distance, coil number, and feeder diameter did not significantly differ between recanalized and reperfused PAVMs. There was a significant (P = .014) difference in retreatment success; retreatment was successful in 84% (n = 27) of 32 recanalized PAVMs but only 44% (n = 4) of nine reperfused PAVMs. Recanalization through previously placed coils is the most common pattern of PAVM persistence and responds best to retreatment. Pulmonary-to-pulmonary reperfusion is less common and more difficult to re-treat successfully. Online supplemental material is available for this article.

Reconstruction of pulmonary artery with porcine small intestinal submucosa in a lamb surgical model: Viability and growth potential

This study investigated the time-dependent remodeling and growth potential of porcine small intestine submucosa as a biomaterial for the reconstruction of pulmonary arteries in a lamb model. Left pulmonary arteries were partially replaced with small intestine submucosal biomaterial in 6 lambs. Two animals each were humanely killed at 1, 3, and 6 months. Computed tomographic angiography, macroscopic examination of the implanted patch, and microscopic analysis of tissue explants were performed. All animals survived without complications. Patency and arborization of the pulmonary arteries were detected 6 months after implantation. There was no macroscopic narrowing or aneurysm formation in the patch area. The luminal appearance of the patch was similar to the intimal layer of the adjacent native pulmonary artery. Scanning electron microscopy showed that the luminal surface of the patch was covered by confluent cells. Immunohistochemical examination confirmed endothelialization of the luminal side of the patch in all of the explanted patches. The presence of smooth muscle cells in the medial layer was confirmed at all time points; however, expression of elastin, growth of the muscular layer, and complete degradation of patch material were detectable only after 6 months. The presence of c-Kit-positive cells suggests migration of multipotent cells into the patch, which may play a role in remodeling the small intestine submucosal biomaterial. Our data confirmed that remodeling and growth potential of the small intestine submucosal biomaterial are time dependent. Additional experiments are required to investigate the stability of the patch material over a longer period.

Wegener’s Granulomatosis Presenting with Bilateral Excavated Nodules

Wegener’s granulomatosis (WG) is a systemic inflammatory disease whose histopathologic features often include necrosis, granuloma formation, and vasculitis of small-to-medium-sized vessels. We report a new case of Wegener’s granulomatosis occurring in a 41-year-old man who was admitted for respiratory symptoms, fever, asthenia, night sweats and weight loss since one month. Chest X-ray and computed tomography showed multiple bilateral pulmonary excavated lesions. A trransparietal lung biopsy was performed. Histological examination showed an area of necrosis, surrounded by a palisade of histiocytes. Some of the histiocytes were multinucleated and formed true granulomas within the wall of the adjacent pulmonary artery. Serology was strongly positive for ANCA. A diagnosis of Wegener granulomatosis was conducted and the patient was started on cyclophosphamide and methylprednisolone as an initial treatment, with a favorable evolution.

Flow-sensitive four-dimensional magnetic resonance imaging facilitates and improves the accurate diagnosis of partial anomalous pulmonary venous drainage

To assess if flow-sensitive four-dimensional velocity-encoded cine magnetic resonance imaging adds value in diagnosing patients with suspected partial anomalous pulmonary venous drainage. In six patients with echocardiographically suspected partial anomalous pulmonary venous drainage, anatomy was evaluated using standard magnetic resonance imaging including angiography. Functional analysis included shunt calculations from flow measurements. We used four-dimensional velocity-encoded cine magnetic resonance imaging for visualisation of maldraining pulmonary veins and quantification of flow via the maldraining veins and interatrial communications, if present. In all patients, the diagnosis of partial anomalous pulmonary venous drainage was confirmed by standard magnetic resonance imaging. Shunt volumes ranged from 1.4:1 to 4.7:1. Drainage sites were the superior caval vein (n = 5) or the vertical vein (n = 1). Multiple maldraining pulmonary veins were found in three patients. Pulmonary arteries and veins could be clearly distinguished by selective visualisation using four-dimensional velocity-encoded cine magnetic resonance imaging. Flow measured individually in maldraining pulmonary veins in six patients and across the interatrial communication in three patients revealed a percentage of the overall shunt volume of 30-100% and 58-70%, respectively. Selective visualisation of individual vessels and their flow characteristics by four-dimensional velocity-encoded cine magnetic resonance imaging facilitates in distinguishing adjacent pulmonary arteries and veins and thus improves the accurate diagnosis of maldraining pulmonary veins. By detailed quantification of shunt volumes, additional information for planning of treatment strategies is provided. This method adds clinical value and might replace contrast-enhanced magnetic resonance angiography in these patients in the future.

Tetralogy of Fallot: A Possible Etiology for Narrowing of the Right Pulmonary Artery

Patients with tetralogy of Fallot have right ventricular outflow and pulmonary valve stenosis. They may also have more distal peripheral pulmonary artery stenoses. Peripheral stenosis is believed to be part of the spectrum of the genetic manifestation of tetralogy. Our hypothesis was that narrowing of the right pulmonary artery may be due to compression from the adjacent dilated ascending aorta. We identified 27 patients with tetralogy of Fallot who underwent magnetic resonance imaging scanning postoperatively, most often for evaluation of pulmonary valve stenosis and regurgitation. On the axial image at the level of the right pulmonary artery, we measured the transverse diameters of the ascending and descending aorta, and the minimum and maximum right pulmonary artery diameters. There was a significant correlation between the ratios of the ascending:descending aorta diameters and the maximum:minimum right pulmonary artery diameters. Thus, increasing ascending aorta size is associated with decreasing size of the adjacent right pulmonary artery. In our patient population with tetralogy of Fallot, right pulmonary artery narrowing is at least partly because of compression from the adjacent enlarged ascending aorta.

The effects of hypoxia on the cells of the pulmonary vasculature

Pulmonary hypertension is associated with remodelling of pulmonary vessels. Chronic hypoxia is a common cause of pulmonary hypertension and pulmonary vascular remodelling. Vascular remodelling is characterised largely by fibroblast, smooth muscle and endothelial cell proliferation, which results in lumen obliteration. Chronic hypoxia elicits expression of mitogens, growth factors and cytokines by fibroblasts and endothelial cells, and also the suppression of endothelial nitric oxide synthase. Although hypoxic pulmonary vascular remodelling is associated with medial hypertrophy, many in vitro studies have found that hypoxia does not lead to a direct increase in smooth muscle cell proliferation. This paradox is not well understood and this review aims to examine the various reasons why this might be so. The present authors reviewed data from in vitro studies and also considered whether hypoxia could act on adjacent cells such as fibroblasts and endothelial cells to trigger smooth muscle cell proliferation. It is possible that hypoxia is sensed by fibroblasts, endothelial cells, or both, and relayed to adjacent pulmonary artery smooth muscle cells by intercellular signalling, causing proliferation. The present article reviews the data from in vitro studies of hypoxia on the three cellular components of the pulmonary vascular wall, namely endothelial cells, smooth muscle cells and fibroblasts.

Teratoma occupying the left hemithorax

BackgroundTeratomas are manifested with a great variety of clinical and radiological features, while sometimes they simply represent incidental findings.Case presentationA rare case of benign teratoma of the dermoid cyst type, in an adult 40-year-old female patient, is reported. The patient had presented recurrent pulmonary infections for the previous 2 months, persistent cough, and progressively aggravating dyspnea. A chest X-ray showed total atelectasis of the left lung, and the thoracic CT-scan revealed a huge mass, containing multiple elements of heterogeneous density, probably originating from the mediastinum, occupying the whole left hemithorax. The mass compressed the vital structures of the mediastinum, great vessels and airways, and a chest MRI was performed to accurately detect the anatomical relations. The patient underwent left thoracotomy and the tumor was totally resected. The size of the tumor was extremely large although no invasion to the vessels or to the airway had occurred. Adherence to the adjacent left pulmonary artery and left main bronchus was present, but without erosion or fistulization. The postoperative course was uneventful, while the histological examination confirmed a teratoma.ConclusionA teratoma is a non-homogeneous pathological entity, clinically, radiologically or histologically. It is predominantly diagnosed between the second and fourth decade and the incidence is equal for both sexes. Symptoms are absent in one half of the patients. The case reported is noteworthy as the tumor appeared with total atelectasis of the left lung, and symptoms started 2 months prior to diagnosis. Total removal of the tumor is adequate treatment for this type of teratoma and the prognosis is excellent.

A bronchial epithelium-derived factor reduces pulmonary vascular tone in the newborn rat.

The factors accounting for the maintenance of a low pulmonary vascular resistance postnatally are not completely understood. The aim of this study was to test the hypothesis that bronchial epithelium produces a factor capable of relaxing adjacent pulmonary arterial smooth muscle. We studied fourth-generation intralobar pulmonary arteries and bronchi of 4- to 8-day-old rats. Arteries were mounted on a wire myograph, alone or with the adjacent bronchus. The presence of the attached bronchus significantly reduced pulmonary artery force generation induced by the thromboxane analog (U-46619) or KCl whether the endothelium was present or absent (P < 0.01). The converse was not true in that bronchial force generation was not affected when studied with the adjacent pulmonary artery. Mechanical removal of the bronchial epithelium or addition of the nitric oxide (NO) synthase (NOS) nonspecific (N(G)-monomethyl-l-arginine) or the specific neuronal NOS (7-nitroindazole) inhibitors increased arterial force generation to levels comparable to the isolated artery preparation. Wortmannin, a phosphatidylinositol 3-kinase inhibitor, significantly decreased (P < 0.01) NO release of pulmonary arteries only when the adjacent bronchus was present. We conclude that bronchial epithelium in the newborn rat produces a factor capable of lowering pulmonary vascular muscle tone. This relaxant effect can be suppressed by NOS and phosphatidylinositol 3-kinase kinase inhibition, suggesting an action via NOS phosphorylation and NO release. We speculate that such a mechanism may be operative in vivo and plays an important role in control of pulmonary vascular resistance in the early postnatal period.

Hypoxic pulmonary artery fibroblasts trigger proliferation of vascular smooth muscle cells: role of hypoxia-inducible transcription factors.

Chronic lung hypoxia causes vascular remodeling with pulmonary artery smooth muscle cell (SMCPA) hyperplasia, resulting in pulmonary hypertension and cor pulmonale. We investigated SMCPA and pulmonary artery adventitial fibroblasts (FBPA) for their proliferative response to hypoxia. Strong SMCPA growth occurred under hypoxic conditions in SMCPA/FBPA co-cultures, but not in SMCPA monocultures. SMCPA growth was fully reproduced by transferring serum-free supernatant from hypoxic cultured FBPA to normoxic SMCPA. Hypoxia-inducible-transcription-factor subtypes (HIF-1alpha, HIF-2alpha, HIF-3alpha) and its dependent target genes, carrying the hypoxia-responsive-element as regulatory component, were strongly activated in both hypoxic FBPA and SMCPA. HIF-transcription-factor decoy technique, employed to FBPA during hypoxic culturing, blocked the mitogenic activity of FBPA conditioned medium on SMCPA. The data suggest that hypoxia-driven gene regulation in pulmonary artery fibroblasts results in a mitogenic stimulus on adjacent pulmonary artery smooth muscle cells, and HIF-transcription-decoy may offer a new therapeutic approach to suppress these events.

Apoptosis and regulation of Bax and Bcl-X proteins during human neonatal vascular remodeling.

To verify that apoptosis is one of the possible mechanisms of neonatal vascular remodeling during the transition from fetal to neonatal circulation, we assayed for apoptosis and evaluated the expression of apoptosis-regulatory proteins in umbilical vessel versus ascending aorta, ductus arteriosus (DA) versus adjacent pulmonary artery and aorta, or aorta versus its branching arteries. Twenty-two umbilical cords (UCs), 6 DAs with adjacent aortas and pulmonary arteries, and 4 aortic arches with their branching great arteries were obtained from neonates. Smooth muscle cell (SMC) apoptosis in umbilical vessels was identified in all UCs. The expressions of Bax and Bcl-X were stronger in umbilical artery than in the neonatal aorta, but Bcl-2 was weak in both arteries in immunohistochemistry. In the immunoblot analysis of UCs, the expression of the proapoptotic short isoform of Bcl-X was stronger than in other tissue, and caspase-3 was selectively activated, whereas it was not in the other components of the cardiovascular system. In contrast, the expression patterns of the FasAg and Fas ligand were similar in umbilical artery and aorta. Regulation of Bcl-2 family proteins was also observed in other vascular sites at which SMCs undergo apoptosis on hemodynamic changes during birth, such as the DA and the branching points of the great arteries from the aortic arch. Apoptosis is involved in the regression of human umbilical vessels and the DA and in the remodeling of the branching great arteries during the neonatal period, when Bcl-2 family proteins are likely to play a key role.