• Physical Therapy Rehabilitation Science
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• v.4 no.1
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• pp.17-21
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• 2015

Objective: In this study, we aimed to test the hypothesis that aerobic exercise might exert its cardio-protective effect by preventing oxidative stress and improving cardiac function in rat models with doxorubicin-induced cardiomyopathy. Design: Randomized controlled trial. Methods: We randomly divided experimental rats into four groups: the normal group was used as a non-cardiomyopathy normal control (n=10); the control group included non-aerobic exercise after doxorubicin-induced cardiomyopathy (n=10); the experimental group I included aerobic exercise (3 m/min) after doxorubicin-induced cardiomyopathy (n=10); and experimental group II included aerobic exercise (8 m/min) after doxorubicin-induced cardiomyopathy. Rats in the treadmill training groups underwent treadmill training, which began at 2 weeks after the first intraperitoneal injection. At the end of the exercise period, we determined the heart weight change for each rat. Changes in the levels of oxidative stress enzymes (superoxide dismutase [SOD], thiobarbituric acid-reactive substances [TBARS], and catalase) in the cardiac tissue of rats from all four groups were examined at the end of the experiment. Results: Significant cardiac myocyte injury and increase in myocardial TBARS concomitant with a reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Significant cardiac tissue and increase in myocardial TBARS along with reduction in myocardial SOD and catalase were observed following cardiomyopathy (p<0.05). Oxidative parameters were significantly improved in the aerobic exercise groups compared with the control group. Conclusions: These findings indicate that aerobic exercise effectively prevents oxidative stress in rat models with cardiomyopathy.

• Journal of Chest Surgery
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• v.44 no.4
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• pp.294-297
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• 2011

Stress-induced cardiomyopathy is caused by emotional or physical stressors and mimics acute myocardial infarction, though Stress-induced cardiomyopathy is characterized by reversible left ventricular (LV) apical ballooning in the absence of significant coronary artery disease. We describe a 51-year-old male who underwent left upper lobectomy for non-small cell lung cancer, and during which cardiogenic arrest occurred due to stress-induced cardiomyopathy, successfully managed by intra-aortic balloon pumping and extracorporeal membrane oxygenation.

• Archives of Craniofacial Surgery
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• v.11 no.2
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• pp.120-123
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• 2010

Purpose: Epinephrine itself exhibits some cardiotoxicity. However, it rarely induces cardiomyopathy when used in standard doses during surgery for local hemostasis. This paper reports a rare case of stress-induced cardiomyopathy in a young woman after the local infiltration of epinephrine. Methods: Corrective rhinoplasty was planned in a 20-year-old woman. Lidocaine mixed with epinephrine 1:100,000 was injected around the skin of the nose and nasal septum after inducing anesthesia, which resulted in sinus tachycardia and hypotension. Postoperative ECG showed a T wave inversion in the lead V2 and echocardiography revealed transient hypokinesia in the cardiac apex. Cardiac enzyme was mildly elevated. Results: Symptoms and laboratory findings improved considerably, and the patient was discharged from hospital without complications on the sixth day after surgery. Conclusion: The prognosis of catecholamine-induced cardiomyopathy is generally favorable. However, it is important to be aware of the possible adverse effects of local epinephrine infiltration. This case highlights the need for caution when using epinephrine.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.79-83
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• 2006

We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.

• Archives of Plastic Surgery
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• v.38 no.1
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• pp.85-88
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• 2011

Purpose: Takotsubo cardiomyopathy is a relatively uncommon type of stress-induced cardiomyopathy characterized by transient left ventricular regional wall motion abnormalities. Emotional and physical stresses play a key role in this type of cardiomyopathy in postmenopausal women. The current hypothesis is that the syndrome represents a form of catecholamine surge due to stress or epinephrine-mediated acute myocardial stunning. Methods: A 44-year-old woman had suffered premature ventricular contraction following a cardiogenic shock during a breast augmentation surgery under enflurane anesthesia and tumescent solution infiltration. She was treated with cardiopulmonary resuscitation at a local clinic. Then she was brought to the Emergency Department of the authors' hospital. Results: The woman's echocardiogram showed an ejection fraction of 20~25% with associated basal hyperkinesis and left ventricular apical ballooning. The patient was admitted to the ICU and required inotropic support for two weeks. The patient's condition dramatically improved, and her ejection fraction returned to 70%. Conclusion: It is believed that there were multiple triggering factors of the onset of Takotsubo cardiomyopathy in the woman's social and family history, including infiltration of a large volume of the tumescent solution and VPCs induced by enflurane anesthesia without premedication. The importance of careful history-taking, careful pre-operative consultation on psychological suffering especially for breast surgery, premedication before surgery, patient reassurance, and post-operative psychosocial and emotional assistance was again seen in this case.

• Journal of Yeungnam Medical Science
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• v.33 no.2
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• pp.125-129
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• 2016

Stress induced cardiomyopathy (SC) is characterized by transient left ventricular (LV) dysfunction in the absence of coronary artery disease. We report on a patient with panhypopituitarism who developed SC resulting from withdrawal of hormonal replacement therapy (HRT). A 52-year-old male visited our hospital for progressively worsening dyspnea. The patient had discontinued HRT 7 days ago, which had been administered for 18 months after transsphenoidal adenomectomy for pituitary macroadenoma. Initial electrocardiogram showed marked sinus bradycardia. Transthoracic echocardiography showed apical ballooning with an LV ejection fraction of 25%. No significant obstructive lesions were observed on coronary angiography. With a clinical diagnosis of SC associated with panhypopituitarism, HRT was restarted, including glucocorticoid and thyroxine, along with standard heart failure management. His LV function had normalized at 2-month follow-up. He remains asymptomatic and administration of beta-blocker and angiotensin converting enzyme inhibitor were discontinued He currently only requires HRT.

• Biomolecules & Therapeutics
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• v.21 no.5
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• pp.371-380
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• 2013

Doxorubicin is still main drug in chemotherapy with limitation of use due to adverse drug reaction. Increased oxidative stress and alteration of nitric oxide control have been involved in cardiotoxicity of doxorubicin (DOX). A Disintegrin And Metalloproteinase (ADAMs) are transmembrane ectoproteases to regulate cell-cell and cell-matrix interactions, but role in cardiac disease is unclear. The aim of this study was to determine whether DOX activates peroxynitrite and ADAM 10 and thus ADAM and matrix metalloproteinase (MMP) induce cardiac remodeling in DOX-induced cardiomyopathy. Adult male Sprague-Dawley rats were subjected to cardiomyopathy by DOX (6 times of 2.5 mg/kg DOX over 2-weeks), and were randomized as four groups. Then followed by 3, 5, 7, and 14 days after cessation of DOX injection. DOX-injected animals significantly decreased left ventricular fractional shortening compared with control by M-mode echocardiography. The expressions of cardiac nitrotyrosine by immunohistochemistry were significant increased, and persisted for 2 weeks following the last injection. The expression of eNOS was increased by 1.9 times (p<0.05), and iNOS was marked increased in DOX-heart compared with control (p<0.001). Compared to control rats, cardiac ADAM10- and MMP 9- protein expressions increased by 20 times, and active/total MMP 9 proteolytic activity showed increase tendency at day 14 after cessation of DOX injection (n=10, each group). DOX-treated $H_9C_2$ cell showed increased ADAM10 protein expression with dose-dependency (p<0.01) and morphometric changes showed the increase of ventricular interstitial, nonvascular collagen deposition. These data suggest that activation of cardiac peroxynitrite with increased iNOS expression and ADAM 10-dependent MMP 9 expression may be a molecular mechanism that contributes to left ventricular remodeling in DOXinduced cardiomyopathy.

• 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 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.

• 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.