• Journal of Chest Surgery
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• v.40 no.9
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• pp.600-606
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• 2007

Background: Infective endocarditis shows high surgical mortality and morbidity rates, especially for aortic endocarditis. This study attempts to investigate the clinical characteristics and operative results of isolated aortic endocarditis. Material and Method: From July 1990 to May 2005, 25 patients with isolated aortic endocarditis (Group I, male female=18 : 7, mean age $43.2{\pm}18.6$ years) and 23 patients with isolated mitral endocarditis (Group II, male female=10 : 13, mean age $43.2{\pm}17.1$ years) underwent surgical treatment in our hospital. All the patients had native endocarditis and 7 patients showed a bicuspid aortic valve in Group I. Two patients had prosthetic valve endocarditis and one patients developed mitral endocarditis after a mitral valvuloplasty in Group II. Positive blood cultures were obtained from 11 (44.0%) patients in Group I, and 10 (43.3%) patients in Group II, The pre-operative left ventricular ejection fraction for each group was $60.8{\pm}8.7%$ and $62.1{\pm}8.1%$ (p=0.945), respectively. There was moderate to severe aortic regurgitation in 18 patients and vegetations were detected in 17 patients in Group I. There was moderate to severe mitral regurgitation in 19 patients and vegetations were found in 18 patients in Group II. One patient had a ventricular septal defect and another patient underwent a Maze operation with microwaves due to atrial fibrillation. We performed echocardiography before discharge and each year during follow-up. The mean follow-up period was $37.2{\pm}23.5$ (range $9{\sim}123$) months. Result: Postoperative complications included three cases of low cardiac output in Group I and one case each of re-surgery because of bleeding and low cardiac output in Group II. One patient died from an intra-cranial hemorrhage on the first day after surgery in Group I, but there were no early deaths in Group II. The 1, 3-, and 5-year valve related event free rates were 92.0%, 88.0%, and 88.0% for Group I patients, and 91.3%, 76.0%, and 76.0% for Group II patients, respectively. The 1, 3-, and 5-year survival rates were 96.0%, 96.0%, and 96.0% for Group I patients, and foo%, 84.9%, and 84.9% for Group II patients, respectively. Conclusion: Acceptable surgical results and mid-term clinical results for aortic endocarditis were seen.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.