• Tuberculosis and Respiratory Diseases
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• v.69 no.4
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• pp.237-242
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• 2010

Pulmonary vascular disease is a category of disorders, including pulmonary hypertension, pulmonary embolism or chronic thromboembolic pulmonary hypertension, pulmonary vasculitis, pulmonary vascular disease secondary to chronic respiratory disease, and pulmonary vascular tumor and malformations. This article reviews the recent advances in this wide spectrum of pulmonary vascular diseases.

• Korean Journal of Radiology
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• v.23 no.2
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• pp.202-217
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• 2022

Pulmonary arteriovenous malformation (AVM) is a congenital vascular disease in which interventional radiologists can play both diagnostic and therapeutic roles in patient management. The diagnosis of pulmonary AVM is simple and can usually be made based on CT images. Endovascular treatment, that is, selective embolization of the pulmonary artery feeding the nidus of the pulmonary AVM, and/or selectively either the nidus or draining vein, has become a first-line treatment with advances in interventional devices. However, some vascular diseases can simulate pulmonary AVMs on CT and pulmonary angiography. This subset can confuse interventional radiologists and referring physicians. Vascular mimickers of pulmonary AVM have not been widely known and described in detail in the literature, although some of these require surgical correction, while others require regular follow-up. This article reviews the clinical and radiologic features of pulmonary AVMs and their mimickers.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2011.10a
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• pp.554-556
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• 2011

The occurrence of various vascular diseases due to the need for accurate and rapid diagnosis was emphasized. Several limitations to the presence of pulmonary vascular angiography for chest CT imaging was aware of the need for diversity in medical image processing with Insight Toolkit(ITK) suggested pulmonary vascular division. In this paper, by contrast, based on the value of a two-step partitioning of the lungs and blood vessels to perform the process of splitting. Lung area segmentation of each stage image enhancement, threshold value, resulting in areas of interest cut image acquisition and acquired pulmonary vascular division in lung area obtained by applying the fill area. Partitioned on the basis of pulmonary vascular imaging to obtain three-dimensional visualization image of the pulmonary vascular analysis and diagnosis of a variety of perspectives are considered possible.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.6
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• pp.641-647
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• 2016

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high $K^+$ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-$N^G$-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.

• Journal of Chest Surgery
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• v.3 no.2
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• pp.91-106
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• 1970

Two groups of left pulmonary-subclavian artery anastomosis were done in 26 adult mongorel dogs. For the first group. the distal end of the subclnvian artery was nnastomosed to the side of the left pulmonary artery, and for the second group, the subclavian end wns anastomosed to the proximal end of the left lower lobe pulmonary artery. Among them, 6 died of bleeding or anesthetic failure during the day of operation, 10 survived 1 to 106 days and the other 10 were sacrificed at various interval. To investigate the relationship between hemodynamic stress and temporal evolution of the pulmonary vascular lesions. the pulmona try and femoral artery pressures, arteriogram and pathohistological specimens were obtained. The following results were obtained. 1. The postoperative pulmonary artery pressures were within normal limits except 2 dogs in the first group, but in nil 12 dogs of the second group, they were in moderate to maked pulmonary hypertension level. 2 After subclavian pulmonary anastomosis, both groups dogs showed increased femond artery pulse pressure. 3. The pulmonary vascular changes were more severe and appeared earlier in the second group dogs compared with the first group.4. The earliest vascular changes appeared in the media of the small muscular arteries and arterioles. 5. Various vascular chaDges were produced in 2 or 3 months. Thereafter, the changes were stationary. 6. Among the first group, two long-term servivors (No. 705 & 713) which had normal pulmonary artery pressure under the anesthesia, also showed various vascular changes as other pulmonary hypertensive dogs. 7. In the early stage medial hypertrophy. interruptio~l of elastic lamellae were found in the small muscular arteries and arterioles, which were followed by intimal proliferation and thrombosis. These findings may suggest some evidences of trauma to the vessels. 8. Pulmonary arteriograms showed irregularity of the intima of the large and medium sized arteries, abrupt ending of some of the small arteries and narrowing of the anastomosis.

• Journal of Chest Surgery
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• v.9 no.1
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• pp.20-26
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• 1976

Author has performed experimental study on hemodynamic changes of lung following radical hilar stripping and contralateral pulmonary artery ligation. In view of hemodynamic changes in group 1 (right pulmonary artery ligation only) and group 2(left hilar stripping+right pulmonary artery ligation). group 2 showed remarkable decrease rate in oxygen uptake (P<0.001) and total pulmonary blood flow(P<0.001), and the more increase rate in mean pulmonary artery pressure(P<0.02) and total pulmonary vascular resistance (P<0.001). Meanwhile, the decrease percent of left lung vascular resistance was lower than group 1(P<0.001). The hemodynamic changes in group 1 returned to control range two weeks later. In the group 2, two dogs were expired as a result of atelectasis and pulmonary hypertension. Among allying 8 dogs, five months after operation, follow up studies performed in two dogs, which showed normal pulmonary hemodynamics similar to preoperative data. The altered blood gas values and decreased oxygen uptake are more remarkable in denervated lung, which may due to pulmonary hypertension and partly retained more secretion in bronchial trees than usual. Important factors of raising pulmonary vascular resistance and pulmonary artery pressure are considered as the increased blood flow to remaining left lung and dysfunction of pulmonary vascular bed to accept the increased blood flow after denervation. Loss of nerve innervation had a influence, to some extent, to the decrease of oxygen uptake and the increase of pulmonary vascular resistance and pulmonary artery pressure. There can be little question that denervation does impair the pulmonary hemodynamics, however, intact pulmonary nerve innervation is not absolutely essential for survival of the animal.

• Molecules and Cells
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• v.37 no.3
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• pp.196-201
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• 2014

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by the vascular remodeling of the pulmonary arterioles, including formation of plexiform and concentric lesions comprised of proliferative vascular cells. Clinically, PAH leads to increased pulmonary arterial pressure and subsequent right ventricular failure. Existing therapies have improved the outcome but mortality still remains exceedingly high. There is emerging evidence that the seven-transmembrane G-protein coupled receptor APJ and its cognate endogenous ligand apelin are important in the maintenance of pulmonary vascular homeostasis through the targeting of critical mediators, such as Kr$\ddot{u}$ppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and microRNAs (miRNAs). Disruption of this pathway plays a major part in the pathogenesis of PAH. Given its role in the maintenance of pulmonary vascular homeostasis, the apelin-APJ pathway is a potential target for PAH therapy. This review highlights the current state in the understanding of the apelin-APJ axis related to PAH and discusses the therapeutic potential of this signaling pathway as a novel paradigm of PAH therapy.

• Journal of Chest Surgery
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• v.14 no.1
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• pp.9-16
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• 1981

Twenty eight patients with conpnital heart disuse underwent lung biopsy to assets pulmonary obstructive vascular disease at cardiac surpry. Thirteen patients had patent ductus arteriosus, 10, ventricular septal defects and S, atrial septal defects. The aaes were between 2 and 30 years. In patients with patent ductus arteriosus lung biopsy was performed from the IIngular Hlment. The anterior seament of the right upper lobe was blopsled in cases with ventricular septal defect and atrial septal defect. Grading of pulmonary obstructive vascular disease could not be assessed In 9 cases. In 2 cases poor quality of the slides made us impossible to evaluate and In 7 cases there were no suitable small muscular arteries to evaluate in the slides of lung tissue especially taken from the IIngular seament. Nineteen cases were evaluated pulmonary obstructive vascular disease. Among them 17 cases had Heath-Edwards changes of grade 1 and 2 patients had that of grade 3. The thickness of media was measured. It was expressed as percentage of medial thickness to outer diameter of artery. The medial thickness was correlated proportionally with elevation of pulmonary arterial pressure and pulmonary vascular resistance to systemic vascular resistance ratio. There were no complications related to the procedure of lung biopsy.

• Journal of Chest Surgery
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• v.15 no.2
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• pp.183-187
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• 1982

Pulmonary arteriovenous fistula is a congenital vascular malformation In the lung, various synonyms including Pulmonary cavernous vascular malformation, Pulmonary arteriovenous aneurysm, Cavernous hemangioma of the lung0 Pulmonary telangiectasia, Pulmonary hamartoma, etc. The pathogenesis of its symptoms is that unoxygenated, desaturated arterial blood enters into the pulmonary venous system directly. Recently we have experienced one case of the pulmonary arteriovenous fistula which was diagnosed as the pulmonary cystic lesion of the lung preoperatively in 20 years old, 61 kg, male patient. Operation was revealed well circumscribed cystic lesion filled with blood, subpleural and anterior mediobasal location, and bright red colored aspirates on two times needle aspirations. Microscopic finding shows ill circumscribed vascular lesion composed of varying sized blood vessels with irregular thickening of wall and final pathological diagnosis is Pulmonary Arteriovenous Fistula. Basal segmentectomy was done and the patient shows good postoperative course.

• Journal of Chest Surgery
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• v.17 no.3
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• pp.339-345
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• 1984

Thirty four patients with a ventricular septal defect, aged 2 months to 24 years [median 2.33 years], had lung biopsies during open heart procedures to assess the degree of pulmonary vascular disease. The patients were divided into two groups according to their age; group 1 - under 2 years of age [15 patients], and group 2- over 2 years of age [19 patients]. The, pathologic change of the pulmonary arterioles was correlated with pre-operative hemodynamic data in 34 patients. There was no significant correlation between the severity of pulmonary vascular disease according to Heath-Edwards classification and the patients age [X2=1.8381, P=0.1751 ]. There was a significant correlation between degree of medial wall thickness and arteriolar diameter and the level of preoperative peak pulmonary artery pressure and peak systemic artery pressure [Pp/Ps]. Also, there was a good correlation between the preoperative pulmonary vascular resistance and systemic vascular resistance [Rp/Rs]. There was no significant correlation between wall thickness and Pp/Ps, and Rp/Rs below the age of 2 years. We conclude that, in patients over 2 years of age, there was a significant correlation between the medial wall thickness of the pulmonary arteriole and elevation of Pp/Ps and Rp/Rs. This is not true in patients under 2 years of age.