• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.20-21
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• 2001

Free radicals and oxidative stress playa crucial role in the pathophysiology of a broad spectrum of cardiovascular diseases including congestive heart failure, valvular heart disease, cardiomyopathy, hypertrophy, atherosclerosis and ischemic heart disease. We have demonstrated that IH 636 proanthocyanidin extract (GSPE) provides excellent protection against free radicals in both in vitro and in vivo models, and exhibits significantly better efficacy as compared to vitamins C, E and $\beta$-carotene.(omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.1
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• pp.1-14
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• 2014

During long standing hyperglycaemic state in diabetes mellitus, glucose forms covalent adducts with the plasma proteins through a non-enzymatic process known as glycation. Protein glycation and formation of advanced glycation end products (AGEs) play an important role in the pathogenesis of diabetic complications like retinopathy, nephropathy, neuropathy, cardiomyopathy along with some other diseases such as rheumatoid arthritis, osteoporosis and aging. Glycation of proteins interferes with their normal functions by disrupting molecular conformation, altering enzymatic activity, and interfering with receptor functioning. AGEs form intra- and extracellular cross linking not only with proteins, but with some other endogenous key molecules including lipids and nucleic acids to contribute in the development of diabetic complications. Recent studies suggest that AGEs interact with plasma membrane localized receptors for AGEs (RAGE) to alter intracellular signaling, gene expression, release of pro-inflammatory molecules and free radicals. The present review discusses the glycation of plasma proteins such as albumin, fibrinogen, globulins and collagen to form different types of AGEs. Furthermore, the role of AGEs in the pathogenesis of diabetic complications including retinopathy, cataract, neuropathy, nephropathy and cardiomyopathy is also discussed.

• Biomedical Science Letters
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• v.30 no.1
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• pp.10-16
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• 2024

Oxidative stress caused by elevated reactive oxygen species (ROS) in the heart causes various heart diseases. Oxidative stress is known as a factor that causes diseases in various organs as well as the heart. Diseases such as heart failure, myocardial infarction, and cardiomyopathy caused by oxidative stress in the heart can be treated with medication or surgery. Recently, blood cells concentrate (BCC) is used in various treatment areas such as orthopedics, gynecology, and urology. BCC therapy is applied to treatment by concentrating platelets and white blood cells necessary for regeneration through simple centrifugation using autologous blood. As the platelets are activated, many growth factors are released from alpha granules of the platelets. Growth factors such as TGF-β1, PDGF, VEGF, and EGF derived from platelets are involved in various cell signaling pathway. Due to these growth factors, BCC can contribute to tissue regeneration and can treat various diseases. CD34+ cells contained in BCC may also play an important role in tissue regeneration. In this study, we investigated whether BCC has a regenerative effect on heart disease, and if so, what mechanism causes the effect. To observe this, cardiomyocyte cells were treated with H₂O₂ to induce oxidative stress. And the effect was confirmed in the presence or absence of BCC. As a result, in the presence of BCC, the oxidative stress of cardiomyocyte cells was reduced and cell damage was also reduced. These results suggest that BCC therapy can be a new treatment alternative for heart disease.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.2
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• pp.129-143
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• 2024

Sulfur dioxide (SO₂), a novel endogenous gas signaling molecule, is involved in the regulation of cardiac function. Exerting a key role in progression of hyperthyroidism-induced cardiomyopathy (HTC), myocardial fibrosis is mainly caused by myocardial apoptosis, leading to poor treatment outcomes and prognoses. This study aimed to investigate the effect of SO₂ on the hyperthyroidism-induced myocardial fibrosis and the underlying regulatory mechanisms. Elisa, Masson staining, Western-Blot, transmission electron microscope, and immunofluorescence were employed to evaluate the myocardial interstitial collagen deposition, endoplasmic reticulum stress (ERS), apoptosis, changes in endogenous SO₂, and Hippo pathways from in vitro and in vivo experiments. The study results indicated that the hyperthyroidism-induced myocardial fibrosis was accompanied by decreased cardiac function, and down-regulated ERS, apoptosis, and endogenous SO₂-producing enzyme aspartate aminotransferase (AAT)1/2 in cardiac myocytes. In contrast, exogenous SO₂ donors improved cardiac function, reduced myocardial interstitial collagen deposition, up-regulated AAT1/2, antagonized ERS and apoptosis, and inhibited excessive activation of Hippo pathway in hyperthyroid rats. In conclusion, the results herein suggested that SO₂ inhibited the overactivation of the Hippo pathway, antagonized ERS and apoptosis, and alleviated myocardial fibrosis in hyperthyroid rats. Therefore, this study was expected to identify intervention targets and new strategies for prevention and treatment of HTC.

• Journal of Trauma and Injury
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• v.27 no.4
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• pp.229-232
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• 2014

A 55 year-old man hit a vehicle while riding a bicycle. He was diagnosed as left hemopneumothorax, multiple rib fracture, cerebral hemorrhage, and skull fracture. Initially he suffered from hypoxia requiring 100% oxygen with a mechanical ventilator. Finally he became hypotensive. Venovenous extracorporeal membrane oxygenation (ECMO) was initiated to support patient's gas exchange. Because hypotension and left ventricular dysfuction persisted, we converted the mode of support to veno-arterio-venous ECMO. Over four days of intensive care, we could wean off ECMO. The patient went to rehabilitation facility after 45 days of hospitalization. Although trauma and bleeding are considered as relative contraindication of ECMO, careful decision making and management may enable us to use ECMO for trauma-related refractory heart and/or lung failure.

• Investigative Magnetic Resonance Imaging
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• v.18 no.1
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• pp.7-16
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• 2014

Purpose : To evaluate the prevalence and pattern of perfusion defect (PD) on first-pass stress perfusion MR imaging in relation with the degree of left ventricular hypertrophy (LVH) and late gadolinium-enhancement (LGE) in patients with apical hypertrophic cardiomyopathy (APH). Materials and Methods: Cardiac MR imaging with first-pass stress perfusion, cine, and LGE sequence was performed in 26 patients with APH from January 2008 to December 2012. We analyzed a total of 416 segments for LV wall thickness on end-diastolic phase of cine images, and evaluated the number of hypertrophied segment and number of consecutive hypertrophied segment (NCH). We assessed the presence or absence of PD and LGE from all patients. If there was PD, we subdivided the pattern into sporadic (sporadic-PD) or ring (ring-PD). Using univariate logistic method, we obtained the independent predictor for presence of overall PD and ring-PD. Results: PD on stress perfusion MRI was observed in 20 patients (76.9%), 12 of them (60%) showed ring-PD. Maximal LV wall thickness and number of hypertrophied segment were independent predictors for overall PD (all, p < 0.05). NCH with more than 3 segments was an additional independent factor for ring-PD. However, LGE was not statistically related with PD in patients with APH. Conclusion: About three quarters of the patients with APH showed PD, most of them represented as ring-PD. LVH degree or distribution was related with pattern of PD, however, LGE was not related with PD. Therefore, the clinical significance of PD in the patients with APH seems to be different from those with non-APH, and further comparison study between the two groups should be carried out.

• Korean Journal of Radiology
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• v.22 no.1
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• pp.97-105
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• 2021

Objective: The present study aimed to investigate the association between myocardial blood flow (MBF) quantified by dynamic CT myocardial perfusion imaging (CT-MPI) and the increments in heart rate (HR) after stress in patients without obstructive coronary artery disease. Materials and Methods: We retrospectively included 204 subjects who underwent both dynamic CT-MPI and coronary CT angiography (CCTA). Patients with more than minimal coronary stenosis (diameter ≥ 25%), history of myocardial infarction/revascularization, cardiomyopathy, and microvascular dysfunction were excluded. Global MBF at stress was measured using hybrid deconvolution and maximum slope model. Furthermore, the HR increments after stress were recorded. Results: The median radiation dose of dynamic CT-MPI plus CCTA was 5.5 (4.5-6.8) mSv. The median global MBF of all subjects was 156.4 (139.8-180.4) mL/100 mL/min. In subjects with HR increment between 10 to 19 beats per minute (bpm), the global MBF was significantly lower than that of subjects with increment between 20 to 29 bpm (153.3 mL/100 mL/min vs. 171.3 mL/100 mL/min, p = 0.027). This difference became insignificant when the HR increment further increased to ≥ 30 bpm. Conclusion: The global MBF value was associated with the extent of increase in HR after stress. Significantly higher global MBF was seen in subjects with HR increment of ≥ 20 bpm.

• Journal of Yeungnam Medical Science
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• v.30 no.2
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• pp.120-123
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• 2013

The common causes of organic mitral regurgitation (MR) include mitral valve prolapse (MVP) syndrome, rheumatic heart disease, and endocarditis. MR also occurs secondary to dilated cardiomyopathy and coronary artery disease. In acute severe MR, the hemodynamic overload often cannot be tolerated, and mitral valve repair or replacement must be performed immediately. We report herein a case of severe MR due to coronary vasospasm that was confirmed via ergonovine echocardiography in a 70-year-old man. He was scheduled to undergo mitral valve surgery, but it did not push through and he was put on medical therapy.

• Journal of Ginseng Research
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• v.44 no.3
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• pp.483-489
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• 2020

Background: Korean Red Ginseng (KRG) has been known to possess many ginsenosides. These ginsenosides are used for curing cardiovascular problems. The present study show the protective potential of KRG against doxorubicin (DOX)-induced myocardial dysfunction, by assessing electrocardiographic, hemodynamic, and biochemical parameters and histopathological findings. Methods: Animals were fed a standard chow and adjusted to their environment for 3 days before the experiments. Next, the rats were equally divided into five groups (n = 9, each group). The animals were administered with KRG (250 and 500 mg/kg) for 10 days and injected with DOX (20 mg/kg, subcutaneously, twice at a 24-h interval) on the 8th and 9th day. Electrocardiography and echocardiography were performed to study hemodynamics. Plasma levels of superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were measured. In addition, the dose of troponin I and activity of myeloperoxidase in serum and cardiac tissue were analyzed, and the histopathological findings were evaluated using light microscopy. Results: Administration of KRG at a dose of 250 and 500 mg/kg recovered electrocardiographic changes, ejection fraction, fractional shortening, left ventricular systolic pressure, the maximal rate of change in left ventricle contraction (-dP/dt_max), and left ventricle relaxation (-dP/dt_max). In addition, KRG treatment significantly normalized the oxidative stress markers in plasma, dose dependently. In addition, the values of troponin I and myeloperoxidase were ameliorated by KRG treatment, dose dependently. And, KRG treatment showed better histopathological findings when compared with the DOX control group. Conclusion: These mean that KRG mitigates myocardial damage by modulating the hemodynamics, histopathological abnormality, and oxidative stress related to DOX-induced cardiomyopathy in rats. The results of the present study show protective effects of KRG on cardiac toxicity.

• Nuclear Medicine and Molecular Imaging
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• v.43 no.6
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• pp.519-525
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• 2009

Purpose: F-18 fluorodeoxyglucose (FDG) uptake of myocardium is influenced by various factors. Increased glycolysis, and subsequent increased F-18 FDG uptake has been reported in ischemic cardiomyopathy. However, clinical significance of incidentally found myocardial F-18 FDG uptake has not been clarified. We retrospectively reviewed the degree and pattern of myocardial uptake in patients without history of ischemic heart disease who underwent torso F-18 FDG PET/CT for evaluation of neoplastic disease. Materials and Methods: From January 2005 to June 2009, 77 patients who underwent F-18 FDG PET/CT and Tc-99m sestamibi stress/rest SPECT within 3 months were enrolled. Results: Of 77 patients, 55 (71.4%) showed increased F-18 FDG uptake in the myocardium. In this population, 40 showed uniform uptake pattern, while 15 showed focal uptake. In patients with uniform uptake, 17 showed decreased uptake in the septum without perfusion defect on myocardial SPECT. Remaining 23 patients showed uniform uptake, with 1 reversible perfusion defect and 1 fixed perfusion defect. In 15 patients with focal uptake, 9 showed increased F-18 FDG uptake in the base, and only 1 of them showed reversible perfusion defect on myocardial SPECT. In the remaining 6 focal uptake group, 4 had reversible perfusion defect in the corresponding wall, and 1 had apical hypertrophy. Conclusion: We demonstrated that septal defect pattern and basal uptake pattern in the myocardium may represent normal variants. Focal myocardial uptake other than normal variants on oncologic torso F-18 FDG PET/CT with routine fasting protocol may suggest ischemic heart disease, thus further evaluation is warranted.