• Clinical and Experimental Pediatrics
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• v.48 no.8
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• pp.886-893
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• 2005

Purpose : Kawasaki disease is the most common cause of systemic vasculitis in children less than 5 years of age. Recent immunohistochemistry findings suggest that many vascular growth factors play a role in the formation of the coronary artery lesions. Active remodeling of the coronary artery lesions in Kawasaki disease continues in the form of intimal proliferation and neoangiogenesis for several years after the onset of the disease. Intravenous immunoglobulin(IVIG) and corticosteroid have been used in the treatment of Kawasaki disease but the exact mechanism is not clear. We have investigated that IVIG and corticosteroid inhibited vascular endothelial growth factor(VEGF)-induced tube formation of endothelial cells in vitro on Matrigel assay. Methods : Human umbilical vein endothelial cells(HUVECs) were cultured and seeded on Matrigel coated 24 well plates in medium with or without the following agents : VEGF, VEGF plus IVIG, VEGF plus VEGF antibody, VEGF plus methylprednisolone, VEGF, IVIG plus methylprednisolone for 18 hours. The total length of tube structures in each photograph was quantified. Results : IVIG significantly inhibited the proliferation of HUVECs. The inhibitory effect of IVIG was also reversible. In the meantime, VEGF induced the differentiation of HUVECs into capillary like structures on Matrigel, which was inhibited by VEGF antibody in a dose-dependent manner. Interestingly, IVIG and methylprednisolone inhibited VEGF-induced tube formation of HUVECs. IVIG was more effective in inhibition than methylprednisolone alone. Conclusion : We revealed that VEGF induced the differentiation of HUVECs and this effect was inhibited by IVIG and methylprednisolone.

• Clinical and Experimental Pediatrics
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• v.48 no.5
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• pp.539-544
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• 2005

Purpose : The aim of this study was to investigate the pathophysiologic role of serum E-selectin, vascular endothelial growth factor(VEGF)-induced cell adhesion mollecule in Kawasaki disease(KD) and to look for the evidence of direct relationship between the plasma levels of soluble E-selectin and the incidence of coronary artery lesion(CAL). Methods : Changes in plasma levels of sE-selectin(n=98) over time were measured by enzyme-linked immunosorbent assay(ELISA) in 23 patients with acute KD and 25 age-matched febrile children. Results : Compared with control values, the peak levels of plasma sE-selectin were significantly elevated($mean{\pm}S.E$. : $22.89{\pm}12.53ng/mL$ vs $10.65{\pm}3.42ng/mL$, P=0.01) in KD. 5 patients with CAL, plasma sE-selectin levels before treatment were higher than in 18 patients without CAL($mean{\pm}S.E$. : $39.43{\pm}15.08ng/mL$ and $19.00{\pm}8.32ng/mL$, respectively; P=0.01). Plasma sE-selectin declined rapidly in the majority of KD patients regardless of the presence of CAL. Plasma sE-selectin levels after treatment and convalesent period were similar in KD patients with and without CAL. The plasma levels sE-selectin were correlated with those of white blood cell count(r=0.299, P<0.05), CRP(r=0.430, P<0.05), serum albumin(r=-0.483, P<0.05), serum protein(r=-0.502, P<0.05) and hemoglobin(r=-0.372, P<0.05) not with those of ESR, platelet, or duration of fever. There were significant differences in the initial level of serum sE-selectin between KD with and without CAL($mean{\pm}S.E$. : $39.44{\pm}15.08ng/mL$ vs. $19.00{\pm}17.18ng/mL$) in multivariated linear tests. Conclusion : Plasma sE-selectin levels were significantly higher in KD than in other febrile illness. Higher plamsa levels of sE-selectin may have potential as a predictor of CAL in patients with KD.

• Clinical and Experimental Pediatrics
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• v.48 no.7
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• pp.745-752
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• 2005

Purpose : Adolescent obesity is known to be associated with complications such as hypertension, coronary artery disease and insulin resistance. We measured the common carotid artery by ultrasound as a predictor of atherosclerosis, and investigated the relationship between carotid artery parameters and serum cytokines in obese adolescents. Methods : Twenty-nine obese adolescents(16-17 years old, obesity index>130 percent) and twentyseven normal controls were included. Obesity index and body mass index were calculated from their height and weight. Skin fold thickness was measured at the triceps, and fat mass and fat distribution by bioelectrical impedence analysis. Blood pressure was measured at resting state and serum lipid, insulin, and homocysteine levels after a 12-hour fasting period. Intimal wall thickness, systolic and diastolic diameters of the common carotid artery were measured by ultrasound, and compliance and distensibility calculated by equation. Results : Systolic and diastolic diameters of the carotid artery significantly correlated with arm circumference, body mass index, fat distribution and fat mass. The higher systolic blood pressure was, the larger systolic and diastolic diameter. The higher diastolic blood pressure was, the larger carotid intimal thickness. Insulin levels had positive correlations with systolic, diastolic diameters and serum homocysteine level with intimal thickness. Conclusion : The carotid artery diameter significantly increased with the degree of obesity and blood pressure. The carotid intimal wall thickness significantly correlated with diastolic blood pressure. Measurement of carotid artery thickness, insulin and homocysteine levels might be useful to predict the development of coronary artery disease.

• Clinical and Experimental Pediatrics
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• v.48 no.10
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• pp.1139-1142
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• 2005

Purpose : The aim of this study was to investigate the epidemiologic and clinical profiles of Kawasaki disease(KD) in children 8 years of age and older. Methods : For the epidemiologic study of KD in Korea, data of total 15,692 KD patients were collected from 1994 to 2002 on a 3 year basis, by the retrospective survey. Among them, data of 211 KD patients 8 years of age and older were analyzed and compared with those of the KD patients less than 8 years of age. Results : 211 patients 8 years of age and older(1.3% of total KD patients) with the mean age of 9.8 years, included 142 cases aged 8-10 years, 42 cases aged 10-12 years, and 27 cases aged 12 years and older. The male-to-female ratio was 1.9 : 1, the recurrence rate was 3.8%, and the prevalence of cases in sibling was zero. Coronary arterial(CA) abnormalities were detected by echocardiography in 25.4% of the cases, including 7.6% of CA aneurysm cases. There was 1 case complicated by myocardial infarction. Conclusion : Comparing with the data of the KD patients less than 8 years of age, data of 211 patients 8 years of age and older showed significantly higher incidences of CA abnormalities(25.4% : 19.8%) and CA aneurysms(7.6% : 4.0%).

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.53-61
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• 1988

The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.

• The Korean Journal of Physiology
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• v.18 no.1
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

• Journal of Chest Surgery
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• v.37 no.4
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• pp.313-321
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• 2004

Excellent clinical results of the arterial switch operation and the limited availablity of the intraventricular rerouting has recently made an arterial switch operation to become the therapeutic method of choice for the repair of double-outlet right ventricle (DORV) with subpulmonary ventricular septal defect (VSD). The early and midterm outcomes of arterial switch operation for this anomaly were evaluated. Material and Method: Between August 1994 and July 2002, 13 patients underwent an arterial switch operation for the correction of double-outlet right ventricle with subpulmonary VSD at Dong-A university hospital.. The 50% rule was used to define DORV. Median age and mean body weight were 27 days (range, 3-120 days) and 3.8$\pm$0.7kg (range, 2.92-5.3kg) respectively. Aortic arch anomalies were associated in 6 cases (46.2%), which were all repaired through one-stage operation. The relationship of the great arteries were side-by-side in 8 cases (61.5%) and anteroposterior in 5 (38.5%). Coronary artery patterns were 1 LCx-2R in 6 cases, retropulmonary left coronary artery (LCA) in 6, and intramural LCA in 1 respectively. The enlargement of VSD was required in 1 patient and the patch enlargement of right ventricular outflow tract was performed in another one patient. The Lecompte maneuver was used in all but 3 patients with a side by side relationship of the great arteries. Result: Overall postoperative hospital mortality was 23.1 % (3/13). All operative deaths were occurred in the patients with aortic arch anomalies. There was one late death related to the postoperative complication of the central nerve system during the mean follow-up of 41.3$\pm$30.7 months. Pulmonary valvar stenosis (＞30mmHg of pressure gradient) developed in 1 patient (10%) and left pulmonary artery stenosis in 2 (20%), among them, one required reoperation 52 months after repair. There was an asymptomatic patient with moderate aortic regurgitation. 5-year survival rate including operative deaths was 68.3%. Conclusion: Although the operative mortality is high in the patients with aortic arch anomaly, the arterial switch operation for DORV with supbpulmonary VSD can be performed with low operative mortality and low reoperation rate in the patients Without arch anomaly. The arterial switch operation can be considered a good option for this complex anomaly.

• Journal of Chest Surgery
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• v.29 no.10
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• pp.1081-1089
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• 1996

Pulmonary atresia with intact ventricular septum has continued to have a high surgical mortality and morbidity. This mAy attribute to the non-uniformity of the anomaly. We reviewed a total of 34 infants with pulmonary atresla and intact ventricular septum managed in this hospital between 1987 and 1995. Mean age and body weight were 57.2 (range, 3-208) days and 4.1 (range, B.3∼6.8) kg. The preoperative Z-value of the diameter of the tricuspid valve was less than -2 in 85.2% of patients and less than -4 in 33. 3% . It is well correlated w th right ventricular cavity size (n=27. r10.68, p< 0.05). Coronary artery-right ventricular fistulas were identified in 3 patients, and right ventricular dependency was suspected in 1 Over All hospital mortality was 23.5%(8/34), although it decreased to 16.6%(4124) in 1990s. Subsequent procedures were performed in 6 patients between 3 days and 58 months after Initial palliation : one bidirectional cavopulmonary shunt and 1 Fontan operation after systemic-pulmonary shunt, 3 transannular patch + atrial septal defect closure and 1 additional systemic-pulmonary shunt after polmonary valvectomy or valvotomy. Changes of Z-values of the diameter of tricuspid valve have been followed up in 11 patients between 1 and 66 months postoperatively. Z-values were increased In 5 out of 8 transannular right ventriculAr outflow tract enlargement group and in 1 out of 3 pulmonary valvectomy or valvotomy group. Our data suggest that tailoring a treatment to right ventricular cavity size and coronary anom lies may improve the surgical outcome. A Z-value of the tricuspid valve diameter could be used.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.53-61
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• 2005

Background : Cardiac troponin I (cTnI) is a specific marker of myocardial injury. It is known that a higher level of cTnI is associated with a poor clinical outcome in patients with acute coronary syndrome. An elevation in cTnI is also observed in various noncardiac critical illnesses. This study evaluated whether cTnI is useful for predicting the prognosis in noncardiac critically ill patients. Methods : From June 2003 to July 2004 at Gyeongsang National University Hospital, we enrolled 215 patients (male:142, female:73, mean age:$63{\pm}15$ years ) who were admitted for critical illness other than acute coronary syndrome at the medical intensive care unit(ICU). The severity score of critical illness (SAPS II and SOFA) was determined and serum cTnI level was measured within 24 hours after admission to the ICU. The mortality rate was compared between the cTnI-positive (${\geq}0.1{\mu}g/L$) and cTnI-negative ($cTnI<0.1{\mu}g/L$) patients at the $10^{th}$ and $30^{th}$ day after admission to the ICU. The mean cTnI value was compared between the survivors and non-survivors at the $10^{th}$ and $30^{th}$ day after admission to the ICU in the cTnI-positive patients. The correlation between cTnI and the severity of the critical illness score (SAPS II and SOFA) was also analyzed in cTnI-positive patients. Results : 1) The number of cTnI-negative and positive patients were 95(44%) and 120(56%), respectively. 2) The mortality rate at the $10^{th}$ and $30^{th}$ day after admission to the ICU was significantly higher in the cTnI-positive patients (29%, 41%) than in the cTnI-negative patients (12%, 21%)(p<0.01). 3) In the cTnI-positive patients, the mean value of the cTnI at the $10^{th}$ and $30^{th}$ day after admission to the ICU was significantly higher in the non-survivors ($4.5{\pm}9.2{\mu}g/L$, $3.5{\pm}7.9{\mu}g/L$) than in the survivors($1.8{\pm}3.6{\mu}g/L$, $2.0{\pm}3.9{\mu}g/L$) (p < 0.05). 4) In the cTnI-positive patients, the cTnI level was significantly correlated with the SAPS II score (r=0.24, p<0.001) and SOFA score (r=0.30, p<0.001). Conclusion : The cTnI may be a useful prognostic marker in noncardiac critically ill patients.

• Journal of Life Science
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• v.18 no.9
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• pp.1263-1270
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• 2008

The purpose of this study is to investigate the effect of exercise mode and anti-hypertensive drug responding status on the cardiovascular response and perceived exertion in acute coronary syndrome (ACS) patients. Seventy-five patients who participated in six-week exercise rehabilitation therapy performed a treadmill running and a cycle ergometer exercise at intensities of 60%HRR and 85%HRR respectively. Systolic and diastolic blood pressure, mean arterial blood pressure (MAP), rate pressure production (RPP), and ratings of perceived exertion (RPE) were measured. The results of cardiovascular response by the different exercise modes with moderate and intensive intensity of anti-hypertensive drug responder and nonresponder ACS patients were following: First cycle ergometer exercise induced significantly higher SBP, DBP, MAP, RPP and MAP than treadmill running exercise at the intensities of 60%HRR and 85%HRR in both anti-hypertensive responder and nonresponder ACS patients (p<0.05). Secondly anti-hypertensive nonresponder ACS patients had significantly higher DBP and MAP that anti-hypertensive responder ACS patients at all the exercise modes (p<0.05). Finally there was no difference of RPP between anti-hypertensive responder and nomresponder ACS patients, although anti-hypertensive nonresponder ACS patients showed higher blood pressure and RPP than anti-hypertensive responder ACS patients. In conclusion, cycle ergometer induced increased cardiovascular response at same intensities of treadmill running exercise and anti-hypertensive nonresponder ACS patients had even more increased cardiovascular response than anti-hypertensive responder ACS patients with no difference in perceived exertion during exercise. These results suggested that cycle ergometer exercise should be greatly careful with the risk of higher blood pressure, especially for those who are patients with hypertensive blood pressure.