• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.108-111
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• 2018

Extra-corporeal membrane oxygenation (ECMO) has the potential to rescue patients in cardiac arrest or respiratory failure. ECMO has two systems such as veno-arterial and veno-venous circulation. In cardiac arrest resulting from acute myocardial infarction, veno-arterial ECMO is mandatory for systemic circulation and oxygenation. A 75-year old female patient underwent primary coronary intervention for acute myocardial infarction. Despite successful revascularization, recurrent ventricular tachycardia and heart failure were progressing. We performed a veno-arterial ECMO through the femoral artery and vein, then the patient seemed to be stable clinically. However, laboratory studies, echocardiography, and vital signs indicated multi-organ failure and decreasing cardiac function. We found out an error that we performed veno-venous ECMO instead of veno-arterial ECMO. We added a femoral artery cannula and exchange the circuit system to veno-arterial ECMO. While the systemic circulation seemed to be recovered, the left ventricular function was decreased persistently. A hypovolemia resulting from pulmonary hemorrhage was occurred, which lead to ECMO failure. The patient died of cardiac arrest and multi-organ failure 23 hours after ECMO. Because the color of arterial and venous circuits represent the position and efficacy of ECMO, if unexpected or abnormal circuit colors are detected, prompt and aggressive evaluation for ECMO function is mandatory.

• Advances in biomechanics and applications
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• v.1 no.1
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• pp.41-55
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• 2014

Acellular intra-myocardial biomaterial injections have been shown to be therapeutically beneficial in inhibiting ventricular remodelling of myocardial infarction (MI). Based on a biventricular canine cardiac geometry, various finite element models were developed that comprised an ischemic (II) or scarred infarct (SDI) in left ventricular (LV) antero-apical region, without and with intra-myocardial biomaterial injectate in layered (L) and bulk (B) distribution. Changes in myocardial properties and LV geometry were implemented corresponding to infarct stage (tissue softening vs. stiffening, infarct thinning, and cavity dilation) and injectate (infarct thickening). The layered and bulk injectate increased ejection fraction of the infarcted LV by 77% (II+L) and 25% (II+B) at the ischemic stage and by 61% (SDI+L) and 63% (SDI+B) at the remodelling stage. The injectates decreased the mean end-systolic myofibre stress in the infarct by 99% (II+L), 97% (II+B), 70% (SDI+L) and 36% (SDI+B). The bulk injectate was slightly more effective in improving LV function at the remodelling stage whereas the layered injectate was superior in functional improvement at ischemic stage and in reduction of wall stress at ischemic and remodelling stage. These findings may stimulate and guide further research towards tailoring acellular biomaterial injectate therapies for MI.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.533-543
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• 2021

Myocardial fibrosis (MF) is the result of persistent and repeated aggravation of myocardial ischemia and hypoxia, leading to the gradual development of heart failure of chronic ischemic heart disease. Triptolide (TPL) is identified to be involved in the treatment for MF. This study aims to explore the mechanism of TPL in the treatment of MF. The MF rat model was established, subcutaneously injected with isoproterenol and treated by subcutaneous injection of TPL. The cardiac function of each group was evaluated, including LVEF, LVFS, LVES, and LVED. The expressions of ANP, BNP, inflammatory related factors (IL-1β, IL-18, TNF-α, MCP-1, VCAM1), NLRP3 inflammasome factors (NLRP3, ASC) and fibrosis related factors (TGF-β1, COL1, and COL3) in rats were dete cted. H&E staining and Masson staining were used to observe myocardial cell inflammation and fibrosis of rats. Western blot was used to detect the p-P65 and t-P65 levels in nucleoprotein of rat myocardial tissues. LVED and LVES of MF group were significantly upregulated, LVEF and LVFS were significantly downregulated, while TPL treatment reversed these trends; TPL treatment downregulated the tissue injury and improved the pathological damage of MF rats. TPL treatment downregulated the levels of inflammatory factors and fibrosis factors, and inhibited the activation of NLRP3 inflammasome. Activation of NLRP3 inflammasome or NF-κB pathway reversed the effect of TPL on MF. Collectively, TPL inhibited the activation of NLRP3 inflammasome by inhibiting NF-κB pathway, and improved MF in MF rats.

• Korean Journal of Veterinary Research
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• v.37 no.3
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• pp.669-685
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• 1997

The present study was performed to evaluate the effects of xylazine and tiletamine + zolazepam on echocardiograms before and after experimental myocardial infarctions in clinically normal dogs taken preliminary examinations related to cardiac function. The results are as follows. With xylazine administration, left ventricle end-diastolic dimension, left ventricle end-systolic dimension, left atrium/aorta, ejection time and velocity of circumferential fiber shortening increased and mitral valve CD slope, % delta D decreased(p<0.01). In tiletamine+zolazepam administered group, interventricular septum amplitude(p<0.01), mitral valve DE slope(p<0.05) and ejection time(p<0.01) decreased and left atrium/aorta, ejection time also decreased compared with xylazine group(p<0.01). In 48 hours after experimental myocardial infarction group, anterior aortic wall amplitude decreased compared with control, xylazine, tiletamine + zolazepam group, respectively(p<0.01). Posterior aortic wall amplitude decreased compared with control(p<0.01). Left ventricle end systolic dimension increased compared with control and tiletamine + zolazepam group, respectively(p<0.01). Left ventricular posterior wall end systolic dimension decreased compared with control(p<0.01). Left ventricular posterior wall amplitude decreased compared with control and tiletamine+zolazepam group(p<0.01). Left atrium/aorta decreased compared with xylazine group(p<0.01). % thickening left ventricular posterior wall decreased compared with control(p<0.05). % delta D decreased compared with control and tiletamine+zolazepam group(p<0.01). Ejection time decreased compared with xylazine(p<0.01). Velocity of circumferential fiber shortening increased compared with control and tiletamine + zolazepam group(p<0.01). With xylazine administration 48 hours after experimental myocardial infarction, anterior aortic wall amplitude, posterior aortic wall amplitude decreased compared with control(p<0.01). Left ventricle end-diastolic dimension increased compared with control(p<0.01). Left ventricle end-systolic dimension increased compared with control and tiletamine + zolazepam group, respectively(p<0.01). Left ventricular posterior wall end-systolic dimension and left ventricular posterior wall end-diastolic dimension decreased compared with control(p<0.01). Left atrium/aorta decreased compared with xylazine group(p<0.01). % thickening left ventricular posterior. wall(p<0.05) and % delta D(p<0.01) decreased compared with control. Velocity of circumferential fiber shortening increased compared with tiletamine + zolazepam group(p<0.01). With tiletamine + zolazepam administration 48 hours after experimental myocardial infarction, anterior aortic wall amplitude decreased compared with control, xylazine and tiletamine+zolazepam group, respectively(p<0.01). Posterior aortic wall amplitude decreased compared with control(p<0.01). Left ventricle end-systolic dimension increased compared with control and tiletamine+zolazepam group(p<0.01). Left ventricular posterior wall end-systolic dimension, left ventricular posterior wall end-diastolic dimension and interventricular septum amplitude decreased compared with control(p<0.01). Left atrium/aorta decreased compared with xylazine group(p<0.01). % delta D decreased compared with control and tiletamine + zolazepam group(p<0.01). Ejection time decreased compared with xylazine group and velocity of circumferential fiber shortening increased compared withtiletamine+zolazepam group(p<0.01). Conclusively, echocardiography was proved to be a useful, diagnostic, non-invasive and simple method for establishing the diagnosis of myocardial infarction and evaluating the effects of drug on cardiac function before and after myocardial infarction.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.6
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• pp.511-518
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• 2022

Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by neogambogic acid. In conclusion, neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.

• Journal of Korean society of Dental Hygiene
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• v.21 no.6
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• pp.751-761
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• 2021

Objectives: The purpose of this study was to examine the relationship between limited oral function and cardiovascular disease in adults over 40 years of age. Methods: Data from the Seventh Korean National Health and Nutrition Examination Survey (2016-2018) was used. In this study, 8,766 adults over the age of 40 years were included as study subjects. They completed a health survey which included current prevalence of hypertension, stroke, myocardial infarction, and angina pectoris, as well as information about blood tests, physical measurements, and oral examinations. Statistical analyses were carried out using complex sample cross-tabulation analysis, general linear model, and logistic regression analysis. Results: The study showed that limited oral function was experienced by patients with stroke (61.3%), myocardial infarction (49.1%), cardiovascular disease (38.5%), hypertension (38.1%), and angina (36.4%) (p<0.05). In patients with stroke, the risk of limited oral function was 2.393 times higher than in patients without stroke. Patients with hypertension were 1.233 times more at risk of speaking difficulty than those without hypertension. Conclusions: Limited oral function is associated with cardiovascular disease. To improve oral health, it is necessary to provide integrated, health-based oral care.

• 대한핵의학회:학술대회논문집
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• 1998.11a
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• pp.443-449
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• 1998

• Journal of Chest Surgery
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• v.21 no.2
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• pp.246-253
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• 1988

An in vitro model providing with a recirculating perfusion apparatus using an isolated canine heart and its autogenous blood, which was prepared for study of myocardial protection method. This apparatus was easily used by quick connect system and maintained well heart function for about 2 hours. The Langendorff perfusion was initiated for a 10 minute period by introducing perfusate at 37` into the aorta from aortic reservoir located 100 cm above the heart. The isolated perfused working canine heart model was a left heart preparation in which oxygenated perfusion medium [at 37K] entered the cannulated left atrium at a constant flow rate [900ml/ min] under 20 mmHg overflow system and was spontaneously ejected[no electrical pacing] via an cannula against a hydrostatic pressure of 80 cm H2O. During this working period, various indices of cardiac function were measured. The cardiac functions were stable for over 2 hours with perfusion of Krebs-Henseleit solution and autologous blood[1:1] mixture in volume and maintained heart rate ]]3-122/bpm peak systolic pressure 109-113 mmHg, cardiac output 900 ml / min and left atrial mean pressure 8-9 mmHg. In this model, the efficiency of myocardia] protection could be easily measured by means of functional, enzymatic, biochemical and ultrastructural assessment. And also, we believe this model to be a useful assessment screening model of recovery state after long duration of myocardial preservation of donor heart without difficult transplantation procedures.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.329-334
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• 2019

Diabetes is associated with an increased risk of cardiovascular complications. Dipeptidyl peptidase-4 (DPP-IV) inhibitors are used clinically to reduce high blood glucose levels as an antidiabetic agent. However, the effect of the DPP-IV inhibitor gemigliptin on ischemia/reperfusion (I/R)-induced myocardial injury and hypertension is unknown. In this study, we assessed the effects and mechanisms of gemigliptin in rat models of myocardial I/R injury and spontaneous hypertension. Gemigliptin (20 and 100 mg/kg/d) or vehicle was administered intragastrically to Sprague-Dawley rats for 4 weeks before induction of I/R injury. Gemigliptin exerted a preventive effect on I/R injury by improving hemodynamic function and reducing infarct size compared to the vehicle control group. Moreover, administration of gemigliptin (0.03% and 0.15%) powder in food for 4 weeks reversed hypertrophy and improved diastolic function in spontaneously hypertensive rats. We report here a novel effect of the gemigliptin on I/R injury and hypertension.

• 대한핵의학회:학술대회논문집
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• 2000.05a
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• pp.76.2-76.2
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• 2000