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OBJECTIVE: Infection is a major cause of mortality in the first year following single lung transplantation and is a distinct risk factor for the development of obliterative bronchiolitis. However, little is known about changes in pulmonary vascular activity in the setting of infection, which might affect and limit function of the graft. Therefore, the aim of this study was to determine how acute infection altered pulmonary arterial reactivity in single lung allografts. Such information could help to develop better diagnostic and therapeutic targets to improve outcome when grafts become infected. METHODS: Following single lung transplantation, dogs were immunosuppressed with methylprednisolone acetate, cyclosporine and azathioprine. On postoperative day 5, infection was induced in one group of dogs by endobronchial inoculation of antibiotic resistant Eschericia coli (infection group, n=5); in the second group, the same amount of culture media without bacteria was flushed into the bronchus (control group, n=4). All animals were medicated under the same drug protocol. On postoperative day 8, lungs were removed, reviewed for histological assessment, pulmonary arteries were isolated, cut into rings and suspended for pharmacological characterization in organ chambers. RESULTS: With acute infections, contractions to phenylephrine and angiotensin-1, but not endothelin-1, were reduced in pulmonary arteries with but not without endothelium. Inhibition of nitric oxide synthase with N(G)-monomethyl-L-arginine, monoacetate salt (L-NMMA) restored these contractions. Endothelium-dependent relaxations to adenosine diphosphate and calcium ionophore, which stimulate release of endothelium-derived nitric oxide by a receptor and non-receptor mediated process, respectively, were not different between groups. Relaxations to nitric oxide also were not different between groups. CONCLUSION: These results suggest that acute infection selectively reduces contractions of pulmonary arteries in part through receptor-mediated release of nitric oxide from the endothelium. Inhibiting nitric oxide during episodes of acute infection may help to improve graft perfusion during episodes of acute infection.

Advanced atherosclerosis is often associated with dystrophic calcification and remodeling of extracellular matrix of vascular wall. Recently many studies have documented a general relationship between calcification and severity of coronary disease, and discussed the feasibility of electron beam computed tomography for detecting and quantifying the coronary artery calcification in the patients. The present study investigated the expression and the localization of osteopontin, one of noncollagenous bone matrix protein, within the calcified coronary arteries. Autopsy-derived coronary artery specimens were scanned and reconstructed to visualize the pattern of coronary calcification using a novel microscopic computed tomography technique. The localization of the osteopontin were evaluated by immunohistochemial stain with LF7. The present study showed that the pattern of coronary calcification is variable and the expression of osteopontin is localized mainly to calcified lesion. The smooth muscle cells in addition to macrophage expressed osteopontin protein in human coronary atherosclerotic plaques. Soluble osteopontin released near to the sites of vascular calcification may represent an adaptive mechanism aimed at regulating the process of vascular calcification.

BACKGROUND: Experiments were designed to determine expression of type II (iNOS) and type III (ecNOS) nitric oxide synthase in lung parenchyma and systemic endothelial cells with rejection and/or infection of single lung allografts. METHODS: After single lung allotransplantation, dogs were maintained on standard triple immunosuppressive therapy for 5 days and then placed into one of three groups. Group I (n=4) was maintained on immunosuppressants, group II (n=7) immunosuppression was withdrawn to allow acute rejection of the allograft, and group III (n=6) infection was induced by bronchoscopic inoculation of Escherichia coli. RESULTS: At postoperative days 7-9, no histological evidence of rejection or infection was observed in transplanted lungs of group I. In lungs of group II, rejection ranged from mild to severe; in lungs of group III, infection was severe. Some animals had both rejection and infection (n=8) and were studied separately. Plasma levels of nitric oxide increased comparably with rejection and/or infection compared to preoperative values. Expression of mRNA for ecNOS decreased significantly in lung parenchyma but not in aortic endothelial cells from dogs of groups II and III. However, expression of mRNA for iNOS increased with both rejection and/or infection in both lung parenchyma and aortic endothelial cells. CONCLUSIONS: iNOS is induced locally within the graft and systemically in aortic endothelial cells with rejection and/or infection of lung allografts. Plasma levels of nitric oxide are elevated with both rejection and infection and may not be useful in the differential diagnosis of these processes after lung transplantation.

Experiments were designed to characterize endothelin receptors in bronchi and parenchyma of transplanted lungs during acute rejection. Third-order bronchi from autografted or allografted lungs were either cut into rings and suspended in organ chambers for the measurement of isometric force or frozen for isolation of membrane proteins. Lung parenchyma was prepared for histology or isolation of membrane protein. The grade of rejection was 2.74±0.17 (n=19) in allotransplanted lungs; evidence of infection was present in 58% of the transplanted lungs. In organ chamber experiments, endothelin 1 (which stimulates endothelin A receptors) caused comparable contraction of bronchi from autotransplanted and allotransplanted rejecting lungs. Endothelin 3 (which stimulates endothelin A and B receptors) caused contractions of bronchi from autotransplanted lungs which were not different from those caused by endothelin 1. In contrast, contractions caused by endothelin 3 were reduced in bronchi from rejecting allotransplanted lungs. The magnitude of contractions caused by endothelin 3 was reduced further when infection was present with rejection. Competitive inhibition of 125 I-endothelin 1 by endothelin 3 was significant for a two-site binding model in membranes prepared from all bronchi and lung parenchyma. The total number of binding sites (B max ) was reduced significantly in bronchi and parenchyma from rejecting lungs with or without infection. The relative proportions of high-affinity and low-affinity binding sites did not change. Affinities of both high- and low-affinity receptors were not altered with rejection. These results indicate that at least two subtypes of endothelin receptors are present on canine bronchial smooth muscle and parenchyma. The number of endothelin receptors associated with bronchial contractions is reduced with rejection of lung allografts.

Extralobar pulmonary sequestration, known as accessory lung, is a rare congenital anomaly and intrapericardial lung sequestration is extremely rare. To the best of our knowledge, only four reported cases were intrapericardial. We report a case with intrapericardial extralobar pulmonary sequestration confirmed by operation and morphologic basis.

Palmar hyperhidrosis has a recurrence rate of 0% to 5% after thoracic sympathectomy. From January 1992 to October 1997, thoracic sympathectomy was performed by video-assisted thoracoscopic surgery for hyperhidrosis in 490 patients of whom 5 (2 male and 3 female with a mean age of 20 years) experienced recurrent hyperhidrosis in the early (< 7 days) or late (up to 6 months) postoperative period. All patients had moderate to severe pleural adhesions in the previous sympathectomy sites but no operative complications or crossover to thoracotomy occurred. Surgery resulted in satisfactory outcomes showing that video-assisted thoracoscopic sympathectomy was effective in treating recurrent hyperhidrosis. Prevention of recurrence requires the identification and resection of the second thoracic sympathetic ganglion as well as the Kuntz fibers.

A 34-year-old woman was admitted to the hospital because of recently aggravated right heart failure without angina for 5 months. When she was 25 years old, patch repair with Polytetrafluoroethylene (PTFE) was performed for the secondum type of atrial septal defect (ASD) with moderate pulmonary hypertension. The chest PA, echocardiography and cardiac catheterization at current admission revealed Eisenmenger syndrome without intracardiac shunt. Chest CT scan with contrast revealed markedly dilated pulmonary trunk, both pulmonary arteries and concave disfigurement of the left side of the ascending aorta suggesting extrinsic compression, as well as total occlusion of the ostium of the left main coronary artery that was retrogradly filled with collateral circulation from the right coronary artery. The coronary angiography showed normal right coronary artery and the collaterals that come out from the conus branch to the mid-left anterior descending artery (LAD) and that from distal right coronary artery to the left circumflex artery (LCX) and to the distal LAD, respectively. On aortography, the left main coronary artery was not visualized with no stump, suggestive of total occlusion of the ostium of the left main coronary artery. From our experience, it is possible to say that the occlusion of the ostium of the left main coronary can be induced by the dilated pulmonary artery trunk due to ASD with pulmonary hypertension and that, if the ASD closure was too late, the narrowing or obstruction of the left coronary artery could not be resolved even after operation owing to irreversible pulmonary hypertension.

Mesenchymal hamartoma of the chest wall is a rare tumor with about 53 reported cases in the English literature. We reviewed six chest wall mesenchymal hamartomas in four patients, including two cases with multiple lesions, with specific focus on the radiologic and pathologic correlation. All cases occurred in neonates or infants with ages ranging from seven hours to seven months. They were diagnosed with plain chest radiographs (n=6), ultrasonography (n=2), chest CT scan (n=6), whole body bone scan (n=2) and MRI (n=3). All cases except a small one without cystic change showed the typical features of mesenchymal hamartoma radiographically and pathologically. Radiologically they were well-circumscribed masses with solid and cystic components with multiple fluid-fluid levels in association with single or multiple rib destruction or change. The CT scan showed the typical findings of chest wall hamartoma, and the MR showed heterogeneous signal intensities of the mass on T1- and T2-weighted images. The MR also revealed more concisely a secondary aneurysmal bone cyst formation with multiple fluid-fluid levels on the T2-weighted image. Microscopically, they showed alternating areas of cartilaginous islands and primitive appearing mesenchymal proliferation, which corresponded well with the solid component on the radiologic findings. The areas of bone formation and blood-filled cystic spaces matched the calcified or ossified densities and the cystic components, respectively. A small case without cystic change showed peculiar radiological and pathological findings resembling an osteochondroma. In conclusion, mesenchymal hamartoma of the chest wall in infancy is quite rare and sometimes can be misdiagnosed as malignancy due to the bone-destroying radiographic appearance and the highly cellular and mitotically active microscopic features, unless the radiologists and pathologists are aware of the characteristic clinical, radiological, and pathological findings. Imaging studies can usually make a correct diagnosis with good correlation to the pathologic findings.

Inflammation appears to have a major role in the development of atherosclerosis. Cyclooxygenase-2 (COX-2) is involved in the inflammatory response via the generation of prostanoids that, in turn, are involved in the production of matrix metalloproteinases (MMPs). This study aimed to investigate atherosclerosis in human aortas for in situ tissue distribution of COX-2, MMPs including MMP-9 and membrane type 1 MMP (MT1-MMP), and tissue inhibitor of metalloproteinase-2 (TIMP-2). Immunohistochemical studies were performed on atherosclerotic lesions of aortas from patients with aortic aneurysms (n = 4) and dissections (n = 3) by using antibodies to COX-2, MMP-9, MT1-MMP, and TIMP-2. Control tissues were obtained from traumatically dissected aortas (n = 2). All specimens from diseased aortas had atherosclerotic lesions ranging from fatty streak to atheromatous plaques. In control, there was no expression of COX-2, MMP-9, and MT1-MMP in all aortic layers. Immunoreactivity for COX-2 was predominantly noted in macrophages and smooth muscle cells (SMCs) of the intima including atherosclerotic plaque itself and the medial layer of the plaque base, as well as in SMCs and endothelial lining of the vasa vasorum in the adventitia. Immunoreactivity for MMP-9 and MT1-MMP was found in the same distribution as that of COX-2. Additionally, the expression of TIMP-2 increased in relation to MMP-9 expression. This study demonstrates that COX-2 is coexpressed with MMP-9 and MT1-MMP, not only by macrophages and SMCs in atherosclerotic lesions, but also in endothelial lining of the vasa vasorum of human aortas. Thus, vascular inflammatory reactions may influence extracellular matrix remodeling by coactivation of MMPs in the development of atherosclerosis and, in turn, the progression of disease.

Background . Essential hyperhidrosis is a condition with excessive sweating localized to certain part of the body. A definitive cure can be obtained by upper thoracic sympathectomy. Method . Between June and October 1997, 117 patients with essential hyperhidrosis underwent needle thoracoscopic sympathectomy. Of the 94 patients, 42 were men and 52 women. Their ages ranged from 14 to 63 years, with a mean age of 23 years. Results . There were no mortality or life-threatening complications. Symptomatic improvement was found in 95.7%. Compensatory hyperhidrosis was found in 71.2% of the patients, but in these compensatory hyperhidrosis were mostly tolerable. Conclusions . This therapeutic procedure is minimally invasive and very effective. Further development of the new device and surgical technique are expected to follow.

In the Respiratory Center, Yongdong Severance Hospital, Yonsei University, we performed 10 cases of bilateral lung autotransplantation in mongrel dogs from July 1994 to June 1996, and we have analyzed the hemodynamic changes. Autotransplantation was performed in order to avoid postoperative rejection. The lung was flushed with an Euro-Collins(E-C) solution containing PGE1 which passed through a 10 French catheter inserted into an incision on the anterior half of the pulmonary artery to pulmonary parenchyme, and the vertical incision was made on the anterior half of the left atrium near the proximal part of the pulmonary vein. However, the bronchus was totally divided after clamping both sides. The lung was kept cold (4 degrees C) in the thoracic cavity for an hour by using slushed ice made from an E-C solution. After an hour of cold ischemia, the pulmonary artery was sutured with Prolene 5-0. The pulmonary vein was sutured with Prolene 6-0 by using the continuous everting mattress method. The main bronchus was anastomosed using the telescope method. The arterial oxygen concentration and the pressures in the femoral and pulmonary arteries were measured both preoperatively and postoperatively. There were no significant hemodynamic differences between the preoperative and postoperative mean pulmonary artery pressure (MPAP) (paired t-test, P = 0.05). Lung preservation using a cold (4 degrees C) E-C solution containing PGE1 may be an acceptable method for short-term storage of a lung (for about an hour) in bilateral lung autotransplantation in dogs.

Varicose vein is a very common vascular disease. The most common symptom is leg pain. Long-standing jobs, pregnancy, and a positive family history are the major predisposing or precipitating factors. The mainstay of treatments includes compressive stocking, sclerotherapy, stab avulsion and stripping of vein, ligation of saphenofemoral junction, transilluminated powered phlebectomy, VNUS, and endovenous laser treatment.

Pulmonary asbestosis is defined as bilateral diffuse interstitial fibrosis of the lungs caused by exposure to asbestos. Many occupations are at risk for asbestos exposure, particularly in the mining, milling, manufacturing, construction, shipbuilding, and automotive industries. Therefore, the prevalence of asbestosis should be fairly widespread. The diagnosis of asbestosis can be made on either clinical or pathological grounds. We recently encountered one case of asbestosis which was confirmed histologically. On HRCT, there was ground-glass opacity with irregular linear shadows, subpleural curvilinear lines and parenchymal bands. Neither plaque nor calcification were noted. The histologic findings observed on open-lung biopsy specimen were well in accord with those in HRCT. Many asbestos-coated bodies were present along with black dust.