• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.77-89
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• 1999

Background: High-dose chemotherapy is increasingly employed in many refractory malignant diseases. This therapy has been reported to increase response rate and survival benefits but it is also associated with higher treatment-related morbidity and mortality. We evaluated clinical characteristics and course of the pulmonary toxicity following high-dose chemotherapy with peripheral blood stem cell transplantation. Methods: Ninety-seven patients who had received high-dose chemotherapy with peripheral blood stem cell transplantation were evaluated. Five patients who developed lung lesions which were not related to infection nor primary malignant disease underwent transbronchial lung biopsy. The patients' clinical characteristics, treatments, and prognosis were reviewed retrospectively. Results: Five patients(5.1%) developed idiopathic pneumonia syndrome. The high dose chemotherapy regimens employed were cyclophosphamide, BCNU, and cisplatin in 3 cases, one case of BCNU, etoposide, Ara-C, and cyclophosphamide combination, and a regimen consisting of BCNU, etoposide, Ara-C, and melphalan. The total dose of BCNU used was 300-400 mg/$m^2$ and that of cyclophosphsmide was 6,000 mg/$m^2$. All of 5 patients received radiation therapy before this treatment. After an average duration of 14 weeks (4-26 weeks) of high-dose chemotherapy, patients developed cough, dyspnea and fever. The chest X-rays showed bilateral diffuse infiltration in 3 cases and the focal infiltration in the other 2 cases. All the patients received corticosteroid therapy as a treatment for the lung lesions. Two of them progressed to acute respiratory distress syndrome and died. Three patients recovered without residual lung lesion but one of them died of dilated cardiomyopathy. Conclusion: High-dose chemotherapy with peripheral blood stem cell transplantation especially which containing BCNU regimen may develop idiopathic pneumonia syndrome related to pulmonary toxicity and corticosteroid therapy may be bel1eficial in some cases.

• Journal of Chest Surgery
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• v.30 no.7
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• pp.670-676
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• 1997

The structural failure of the glutaraldehyde-treated xenograft valves has been the primary concern about the limited durability as predicted from the begimling of clinical use, and long-term follow-up has shown a significant incidence of primary tissue failure(PTF) from both biological and mechanical reasons. Twenty-seven patients with the low-profile lonescu-Shiley valves explanted from mitral position for PTF(Group III) were studied on the patient characteristics and valve pathology, and the results were compared with the matched observations of the Haycock(Group I) and of the standard-profile lonesiu-Shiley valves(Group II). Patients were aged 16 to 56 years(mean, 38.0$\pm$ 11.0 years), and the size of the failed mitral bioprosthesis was 30.8$\pm$ 1.3 mm. The hemodynamic consequences were stenosis in 29.6%, insufficiency in 44.4%, mixed steno-insufficiency in 14.8%, together with normal function for the rest of patients of prophylactic re-replacement. Pathology revealed calcification with or without tissue damage in 63.0% and tissue damage with or without calcification in 58.l%, in contrast with the observations of predominant tissue damage(76.8%) over calcification in Group I and of calcification(76.1%) over tissue damage in group II. Although dystrophic calcification has long and repeatedly dealt with patient's young age as a determinant of valve durability, such a characteristic evidence was not reached even in patients with calcified valves. Moreover, the prolonged explantation p riods from the studied on the previous report suggested strongly yet possibly evolving destructive processes among the valves in the remaining patients, and awaits further follow-up. In conclusion, PTF of the xenograft valves seems to result from more complicated biologic and metabolic reasons as well as more complex mecharical factors than the reported, and newer generation prostheses, with tissue preservation with glutaraldehyde, do not likely to provide decisive improvement in the occurrence of structural failurebioprostheses is generally limited to the highly aged.

• Journal of Chest Surgery
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• v.37 no.2
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• pp.131-138
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• 2004

High-flow gas insufflation to get a bloodless field during off-pump coronary artery bypass may have adverse effects on the coronary endothelium. This study was designed (1) to elucidate the effect of carbon dioxide gas insufflations on the coronary endothelium at different flow rates and (2) to assess the protective effect of humidifcation against the coronary endothelial damage. Material and Method: In nine pigs, the left anterior descending coronary artery (LAD) was exposed after a median sternotomy. The LAD was divided into 4 segments and a coronary arteriotomy was made in each LAD segment in the beating heart. The far distal arteriotomy was exposed to room air for 10 minutes and was harvested as a control. Non-humidified carbon dioxide gas at a continuous flow rate of 5 L/min (Group I), humidified carbon dioxide gas at a continuous flow rate of 5 L/min (Group II), and humidified carbon dioxide gas at a continuous flow rate of 10 L/min (Group III) were insufflated for 10 minutes on each coronary arteriotomy site, respectively. After harvesting the coronary segments, hematoxylin-eosin staining, elastic fiber staining, and immunostaining with a CD34 monoclonal antibody were performed to evaluate the depth of endothelial damage and to count the residual endothelial cells, Result: In all three groups (Group I, II, and III), internal elastic laminae were preserved, however, the endothelial layers were significantly damaged by carbon dioxide gas insufflation. The mean percentages of remaining endothelial cells were 20,9$\pm$16.7%, 39.3$\pm$19.6%, and 6.8$\pm$5.3%, in groups I, II, and III, respectively. The percentages of remaining cells were significantly higher in group II than in groups I and III (p=0.008). The percentages of remaining cells were significantly higher in group I than in group III (p=0.008). Conclusions: The harmful effect of carbon dioxide gas insufflation on the coronary endothelium was dependent on the flow rate. The addition of humidification did not protect the coronary endothelium from denudation injury caused by high flow carbon dioxide gas insufflations.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.247-255
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• 2007

Background: Lung injury that follows bypass has been well described. It is manifested as reduced oxygenation and lung compliance and, most importantly, increased pulmonary vascular resistance reactivity; this is a known cause of morbidity and mortality after repair of congenital heart disease. Injury to the pulmonary vascular endothelium, and its associated alterations of endothelin-1, is considered to be a major factor of bypass-induced lung injury. Removing endothelin-1 after bypass may attenuate this response. This study measured the concentration of serum and peritoneal effluent endothelin-1 after performing bypass to determine if endothelin-1 can be removed via peritoneal dialysis. Material and Method: From March 2005 to March 2006, 18 patients were enrolled in this study Peritoneal catheters were placed at the end of surgery. Serum samples were obtained before and after bypass, and peritoneal effluents were obtained after bypass. Endothelin-1 was measured by enzyme linked immunosorbent assay (ELISA). Result: In the patients with a severe increase of the pulmonary artery pressure or flow, the mean preoperative plasma endothelin-1 concentration was significantly higher than that in the patients who were without an increase of their pulmonary artery pressure or flow (4.2 vs 1.8 pg/mL, respectively, p<0.001). The mean concentration of plasma endothelin-1 increased from a preoperative value of $3.61{\pm}2.17\;to\;5.33{\pm}3.72 pg/ml$ immediately after bypass. After peritoneal dialysis, the mean plasma endothelin-1 concentration started to decrease. Its concentration at 18 hours after bypass was significantly lower than the value obtained immediately after bypass (p=0.036). Conclusion: Our data showed that the plasma endothelin-1 concentration became persistently decreased after starting peritoneal dialysis, and this suggests that peritoneal dialysis can remove the circulating plasma endothelin-1.

• Journal of Chest Surgery
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• v.39 no.10 s.267
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• pp.739-748
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• 2006

Background: The purpose of this study is to ascertain the neuroprotective effect of cyclosporin A on the 25-min surgical ischemia model in the spinal cords of rabbits with neuropathological correlation and histoimmunochemical analyses, Material and Method: Thirty-two New Zealand white rabbits were randomly divided into four groups: Rabbits were randomly divided into four groups: the control 12 group (n=8), the control 17 group (n=8), the cyclosporin Cs2 group (n=8), and the cyclosporin Cs7 group (n=8). The 12 group underwent a 25-min aortic cross- clamp without intervention and were sacrificed on the 2nd day postoperatively, while the 17 group underwent a 25- min of aortic cross-clamp without intervention and were sacrificed on the 7th day postoperatively. The Cs2 group received cyclosporin A (25 mg/kg) intravenously 15 min after the 25-min cross-clamp and were sacrificed on the End day postoperatively, while the Cs7 group received cyclosporin A (25 mg/kg) intravenously 15 min after the 25-min cross-clamp and were sacrificed on the 7th day postoperatively. The rabbits underwent 25-min surgical aortic cross-clamp. Neurologic functions were evaluated on the 2nd day and 7th postoperative day using Tarlov scoring system. After scoring neurologic function, all rabbits were sacrificed for histopathologic observation. Result: All rabbits survived the experimental procedure. The values of Tarlov score did not show any differences between the control and cyclosporin groups on the 2nd day. The scores of group Cs7 ($2.75{\pm}0.89$) were significantly higher than those of group 17 ($1.25{\pm}1.39$) on the 7th day (p<0,05). On the histologic exanminations, specimens of the spinal cord showed necrosis and apoptosis. The pathologic scores of group Cs7 ($1,0{\pm}0.53$) was less than those of group 17 ($2.13{\pm}1.36$, p<0.05). TUNEL staing showed apoptosis of the specimen in group 12 and Cs2 but there was no stastically significant difference between groups on the score. There were more overexpression of HSP70 and nNOS in cyclosporine group than in control group. Conclusion: We think that cyclosporin A may decrease neuronal cell death with induced upregulation of HSP70 against 25-min ischemia of the spiral cord in the rabbit.

• Journal of Chest Surgery
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• v.23 no.1
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• pp.95-106
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• 1990

Between May 1979 and April 1989, 213 patients with esophageal injuries visited the Department of the Thoracic and cardiovascular surgery Department, Yonsei University College of Medicine. There were 159 non perforated esophageal injuries accompanied by hematemesis, and 54 perforated esophageal injuries. The causes of non perforated esophageal injuries were Mallory-Weise Syndrome [%], corrosive esophagitis [54], esophageal carcinoma [4], foreign bodies [2], sclerotherapy due to esophageal varices [3]. The causes of perforated esophageal injuries were esophageal anastomosis[13], malignancies[17], esophagoscopy or bougienage[5], chest trauma[5], foreign bodies[5], paraesophageal surgery[3], others[6] In esophageal perforation due to foreign bodies, esophagoscopy or bougienage, there were 6 cervical esophageal perforations and 9 thoracic esophageal perforations. There were no mortalities in the treatment of the cervical esophageal perforations and 5 deaths resulted in the treatment of 9 thoracic esophageal perforations. And four of six patients with thoracic esophageal perforations died in the initiation of treatment over 24 hours, after trauma. There were another 12 deaths in the patients with chest trauma, malignancies or chronic inflammation except esophageal injuries due to foreign bodies or instruments during the hospital stay or less than 30 days after esophageal injuries. One patient with esophageal carcinoma died due to bleeding and respiratory failure after irradiation. Another patient with esophago gastrostomy due to esophageal carcinoma died of sepsis due to EG site leakage. One patient with a mastectomy due to breast cancer followed by irradiation died of sepsis due to an esophagopleural fistula. Two patients with Mallory-Weiss syndrome died; of hemorrhagic shock in one and of respiratory failure due to massive transfusion in the other. One patient with TEF died of respiratory failure and another died of pneumonia and respiratory failure. One patient with esophageal perforation due to blunt chest trauma died of brain damage accompanied with chest trauma.

• Journal of Chest Surgery
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• v.42 no.3
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• pp.384-387
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• 2009

Radial artery aneurysm is an extremely rare disease and this is usually caused by iatrogenic trauma such as arterial cannulation. Most traumatic aneurysms in the extremities are false aneurysms and most cases have occurred at the level of the wrist. Very few true aneurysms of the radial artery have been reported, with most of them being iatrogenic. A right handed 38-year-old female had a true aneurysm of the distal radial artery in the thenar groove of the palm. The patient had a history of excessive handclapping and the injury was suggestive of repetitive occupational injury due to scissoring. She underwent surgical treatment for the aneurysm of the radial artery in the thenar groove of the palm of her hand.

• Journal of Chest Surgery
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• v.28 no.11
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• pp.963-966
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• 1995

Ischemia reperfusion injury occurs in various diseases. The role of oxygen free radicals in IR injury of the lung has been spotlighted and many studies have been performed. In this study, we tried to prepare a stable rat lung model for IR injury, focusing on surrounding conditions as hilar stripped left lung, clamped left pulmonary artery and bronchus,and declamped after determined period was passed, and right main pulmonary aretery was clamped. Arterial blood gas analyes were performed at 1, 10, 20, 30, minutes after reperfusion. Before clamping, PaO2 was 95 to 120 mmHg in all animals. There were six groups; Group I : temperature 15o C, and 120 minutes clamping, Group II: 20 oC, and 120 minutes clamping, Group III : 25 oC, and 120 minutes clamping, Group IV : 15oC, 90 minutes clamping, Group V : 20 oC, 90 minutes clamping,Group VI: 20 oC, 75 minutes clamping. Each groups contained 10 Sprague Dayley rats. The humidity was maintained 100 % as circulation imerged isotonic Hartmann`s solution of the pleural cavity. In group IV, V, and VI, PaO2 decreased significantly in all animals immediately after reperfusion, but 43 % survived till 10 minutes after reperfusion, it was 74.0$\pm$5.7, 73.3$\pm$10.8,and 88.2$\pm$17.7 mmHg. Pulmonary edema was observed histologically in 2/10 animals in group IV, 6/10 in group V , 3/10 in group VI, 9/10 in group I, and the other lungs showed all edema. We established a stable model by setting ischemic time,and temperature, between 75 to 90 minutes,15 to 20o C, and isotemperature Hartmann`s solution immersion of the pleural cavity.

• Journal of Chest Surgery
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• v.32 no.11
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• pp.978-983
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• 1999

Background: Complement activation with transpulmonary leukocyte sequestration is considered a main mediator leading to ischemia-reperfusion lung(I-R) injury. We studied the role of leukocytes in the formation of I-R injury in ovine cardiopulmonary bypass(CPB) model with a membrane oxygenator. Material and Method: Five sheep were used. CPB circuitry consisted of a roller pump(American Optical Corp., Greenwich, CT, USA) and a membrane oxygenator(UNIVOX-IC, Bentley, Baxter Health Corp, Irvine, CA, USA). The CPB time was fixed at 120 min. Ten minutes after the start of CPB, total CPB was established. Thereafter a total CPB of 100 min was performed, followed by another 10 min of partial CPB. The CPB was discontinued and the animals were fully recovered. For measuring left and right atrial leukocyte counts, blood samples were taken before thoracotomy, 5 min and 109 in after the start of CPB, and 30 min and 120 min after weaning. C3a was measured before thoracotomy, 109 min after the start of CPB, and 30 min and 120 min after weaning. Plasma malondialdehyde(MDA) was checked before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. One to two grams of lung tissue were taken for water content measurement before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. Lung biopsy specimens were examined by light and electron microscopy. Result: Of 5 animals, 4 survived the experimental procedures. Of these, 3 animals survived on a long-term basis. No significant differences in transpulmonary gradients of leukocyte were found and no significant complement activation was expressed by C3a levels. MDA level did not show significant changes related to lung reperfusion despite an increase after the start of CPB. On both light and electron microscopic examinations, mild to moderate acute lung change was observed. Interstitial edema, leakage of erythrocytes into the alveolar space and endothelial cell swelling were the main findings. Water content of the lung showed a slight increase after the start of CPB, but there was no statistical significance. Conclusion: These findings indicate that ischemia-repersusion lung injury may not be from complement activation-leukocyte sequestration but from another source of oxygen free radicals related to CPB.

• Journal of Chest Surgery
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• v.30 no.9
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• pp.847-853
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• 1997

Although the effects of adenosine on the heart, including the clinical suppression of cardiac arrhythmias, have been recognized for more than half a century, it is only in the last decade that the therapeutic potential of adenosine has been recognized. The objective of this study was to determine if augmentation of myocardial adenosine levels during global ischemia improves functional recovery after reperfusion. We used to modified Langendonf system to evaluate myocardial protective effect. Isolated rat hearts were subjected to 90 minutes of deep hypothermic arrest(15$^{\circ}C$) with modified St. Thomas'Hospital cardioplegic solution used to provide myocardial protection. Myocardial adenosine levels were augmented during ischemia by providing exogenous adenosine in the cardioplegic solution. Two groups of hearts w re studied: (1) control group(n=10) cardioplegia alone; (2) adenosine group(n=10) adenosine(0.75mg/kg/min) added to the cardioplegic solution. Significantly better percent recovery(p<0.01) in hemodynamics(except heart rate) at 60 minutes after reperfusion was evident compared to baseline values in the adenosine group. (systolic no란ic pressure : 78.5$\pm$3.6% vs 66.6$\pm$5.9%, airtic overflow volume : 61.7$\pm$ 11.6% vs 37.2$\pm$ 15.4%, coronary flow volume 77.1$\pm$7.5% vs 57.2$\pm$ 11.1%, and cardiac output : 65.6$\pm$ 11.5% vs 44.2$\pm$ 12.4%). Heart rate was similar in two groups(94.4$\pm$4.8% vs 95.3 $\pm$ 6.8%). Adenosine groups resulted in significantly rapid recovery time of heart beat after reperEusion(p<0.01) (24.5$\pm$7.6 sec. vs 179.0$\pm$ 131.1sec.). In biochemical study, CPK levels(0.1 $\pm$0.3U/L vs 1.4$\pm$0.8U/L) and lactic acid levels(0.08$\pm$0.Immol/L vs 0.34$\pm$0.2 mmol/L) were significantly low in adenosine groups(p<0.01). We concluded that adenosine included cardioplegia have better recovery effects after r perfusion in myocardial ischemia compared to adenosine free cardioplegia.