• Nutrition Research and Practice
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• v.8 no.4
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• pp.391-397
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• 2014

BACKGROUND/OBJECTIVE: Myocardial cell death due to occlusion of the coronary arteries leads to myocardial infarction, a subset of coronary heart disease (CHD). Dietary fiber is known to be associated with a reduced risk of CHD, the underlying mechanisms of which were suggested to delay the onset of occlusion by ameliorating risk factors. In this study, we tested a hypothesis that a beneficial role of dietary fiber could arise from protection of myocardial cells against ischemic injury, manifested after occlusion of the arteries. MATERIALS/METHODS: Three days after rats were fed apple pectin (AP) (with 10, 40, 100, and 400 mg/kg/day), myocardial ischemic injury was induced by 30 min-ligation of the left anterior descending coronary artery, followed by 3 hr-reperfusion. The area at risk and infarct area were evaluated using Evans blue dye and 2,3,5-triphenyltetrazolium chloride (TTC) staining, respectively. DNA nicks reflecting the extent of myocardial apoptosis were assessed by TUNEL assay. Levels of cleaved caspase-3, Bcl-2, and Bax were assessed by immunohistochemistry. RESULTS: Supplementation of AP (with 100 and 400 mg/kg/day) resulted in significantly attenuated infarct size (IS) (ratio of infarct area to area at risk) by 21.9 and 22.4%, respectively, in the AP-treated group, compared with that in the control group. This attenuation in IS showed correlation with improvement in biomarkers involved in the apoptotic cascades: reduction of apoptotic cells, inhibition of conversion of procaspase-3 to caspase-3, and increase of Bcl-2/Bax ratio, a determinant of cell fate. CONCLUSIONS: The findings indicate that supplementation of AP results in amelioration of myocardial infarction by inhibition of apoptosis. Thus, the current study suggests that intake of dietary fiber reduces the risk of CHD, not only by blocking steps leading to occlusion, but also by protecting against ischemic injury caused by occlusion of the arteries.

• BMB Reports
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• v.49 no.1
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• pp.26-36
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• 2016

Emerging trends for cardiac tissue engineering are focused on increasing the biocompatibility and tissue regeneration ability of artificial heart tissue by incorporating various cell sources and bioactive molecules. Although primary cardiomyocytes can be successfully implanted, clinical applications are restricted due to their low survival rates and poor proliferation. To develop successful cardiovascular tissue regeneration systems, new technologies must be introduced to improve myocardial regeneration. Electrospinning is a simple, versatile technique for fabricating nanofibers. Here, we discuss various biodegradable polymers (natural, synthetic, and combinatorial polymers) that can be used for fiber fabrication. We also describe a series of fiber modification methods that can increase cell survival, proliferation, and migration and provide supporting mechanical properties by mimicking micro-environment structures, such as the extracellular matrix (ECM). In addition, the applications and types of nanofiber-based scaffolds for myocardial regeneration are described. Finally, fusion research methods combined with stem cells and scaffolds to improve biocompatibility are discussed. [BMB Reports 2016; 49(1): 26-36]

• 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.

• Journal of Biomedical Engineering Research
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• v.38 no.6
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• pp.313-320
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• 2017

Myocardial infarction is a disease caused by stenosis of the coronary arteries. The high risk of sudden cardiac death due to myocardial infarction has triggered related researches that have been actively studied so far. However, these studies focused on the clinical results, which are mainly based on observations of symptoms due to infarction through electrocardiograms. Therefore, in this study, we tried to analyze the behavior of heart according to the position and volume of infarction lesion through the computer simulation study using three dimensional ventricular models. In order to implement infarction, commercial software was used to simulate cell necrosis due to blockage of a specific coronary. In addition, the conduction block due to infarction was mimicked by reducing the electrical conduction in the infarcted area, which was 100 times less than the electrical conduction of the whole ventricular lattice implemented by the finite element analysis method. Thus, this study classified the infarcted cases into the upper, middle, lower, and apex according to lattice data of eight different infraction areas. In other words, we assumed that myocardial infarction would have inherent electro-dynamic characteristics depending on the location and extent, and analyzed the ventricular electromechanical responses for infarction lesions using a three dimensional cardiac physiome model. The results showed that the volume of infarction did not directly affect the cardiac responses, but the location of the infarction lesions could influence the ventricular pumping efficiency. These suggest that the occlusion of specific coronary arteries may have a fatal effect on the decline in ventricular performance. In conclusion, although location of myocardial infarction lesions is considered to be an important variable to be considered clinically rather than lesion size, quantitative predictions should be made more in the future considering physiological factors such as lesion location and direction of myocardial fiber at that location.

• Nutrition Research and Practice
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• v.13 no.3
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• pp.205-213
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• 2019

BACKGROUND/OBJECTIVES: Myocardial infarction (MI) is caused by extensive myocardial damage attributed to the occlusion of coronary arteries. Our previous study in a rat model of ischemia/reperfusion (I/R) demonstrated that administration of arabinoxylan (AX), comprising arabinose and xylose, protects against myocardial injury. In this study, we undertook to investigate whether psyllium seed husk (PSH), a safe dietary fiber containing a high level of AX (> 50%), also imparts protection against myocardial injury in the same rat model. MATERIALS/METHODS: Rats were fed diets supplemented with PSH (1, 10, or 100 mg/kg/d) for 3 d. The rats were then subjected to 30 min ischemia through ligation of the left anterior descending coronary artery, followed by 3 h reperfusion through release of the ligation. The hearts were harvested and cut into four slices. To assess infarct size (IS), an index representing heart damage, the slices were stained with 2,3,5-triphenyltetrazolium chloride (TTC). To elucidate underlying mechanisms, Western blotting was performed for the slices. RESULTS: Supplementation with 10 or 100 mg/kg/d of PSH significantly reduces the IS. PSH supplementation (100 mg/kg/d) tends to reduce caspase-3 generation and increase BCL-2/BAX ratio. PSH supplementation also upregulates the expression of nuclear factor erythroid 2-related factor 2 (NRF2), and its target genes including antioxidant enzymes such as glutathione S-transferase mu 2 (GSTM2) and superoxide dismutase 2 (SOD2). PSH supplementation upregulates some sirtuins ($NAD^+$-dependent deacetylases) including SIRT5 (a mitochondrial sirtuin) and SIRT6 and SIRT7 (nuclear sirtuins). Finally, PSH supplementation upregulates the expression of protein kinase A (PKA), and increases phosphorylated cAMP response element-binding protein (CREB) (pCREB), a target protein of PKA. CONCLUSIONS: The results from this study indicate that PSH consumption reduces myocardial I/R injury in rats by inhibiting the apoptotic cascades through modulation of gene expression of several genes located upstream of apoptosis. Therefore, we believe that PSH can be developed as a functional food that would be beneficial in the prevention of MI.

• Journal of Chest Surgery
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• v.35 no.4
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• pp.307-310
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• 2002

The purpose of this presentation is to demonstrate a good results of a second operation, the Waffle procedure, in a patient who did not improve following pericardiectomy. Incomplete parietal pericardiectomy, myocardial fiber atrophy, and unexpected restrictive cardiomyopathy can be considered when the patient\`s symptom does not improve after pericardiectomy is carried out. Constrictive epicarditis is always ruled out. In our case, the patient having constrictive pericarditis combined with pericardial effusion received a pericardiectomy. However, hemodynamics and symptoms of the patient following the operaltion did not improve. However, we experienced a good result following a second operation., the Waffle procedure.

• Korean Journal of Veterinary Service
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• v.41 no.3
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• pp.217-220
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• 2018

A female Russian rat snake, Elaphe schrenckii, was presented for loss of movement. Physical examination showed the swelling in the area of heart. Radiographic examination revealed cardiomegaly, pericardial effusion, and a soft opacity in the area of swelling. Although pericardiocentesis to remove fluid out from the heart as well as vigorous treatments were given to the Russian rat snake, it died during treatments. Postmortem examination confirmed pericardial effusion of pale yellow, translucent fluid with mild dilation of the right atrium and ventricle. Formalin -fixed paraffin embedded tissue sections were stained with routine H&E and the classical von Kossa's method for histopathological demonstration. Histopathological examination revealed multifocal calcification in myocardium and consists of the displacement of muscular fiber by limy deposits. Congestive heart failure was suspicious for the snake when it was alive. In wild reptiles, muscle degeneration has been reported with nutrition disorders but the present case is the first report of myocardial degeneration in a Russian rat snake and contributes to the rare reports of cardiac disease in snakes.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.6
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• pp.517-523
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• 2021

The present study aims to investigate the impact of hydrogen-rich water on the lactic acid level in metformin-treated diabetic rats under hypoxia. Thirty Sprague-Dawley rats were randomly divided into five groups, including normal diet group, and diabetes model (DM) group, DM + metformin treatment (DMM) group, DMM + hypoxia treatment (DMMH) group and DMMH + hydrogen-rich water (DMMHR) group. We found that the levels of lactic acid, pyruvate and lactate dehydrogenase were significantly lower in the blood of DMMHR group than DMMH group. Superoxide dismutase and glutathione levels in liver and heart were significantly higher in DMMH group after hydrogen-rich water treatment, while malondialdehyde and oxidized glutathione levels were decreased in DMMHR group when compared with DMMH group, which indicates that hydrogen-rich water could reduce oxidative stress. qPCR analysis demonstrated that that pro-apoptotic genes Bax/Caspase-3 were upregulated in DM group and metformin treatment suppressed their upregulation (DMM group). However, hypoxic condition reversed the effect of metformin on apoptotic gene expression, and hydrogen-rich water showed little effect on these genes under hypoxia. HE staining showed that hydrogen-rich water prevented myocardial fiber damages under hypoxia. In summary, we conclude that hydrogen-rich water could prevent lactate accumulation and reduce oxidant stress in diabetic rat model to prevent hypoxia-induced damages. It could be served as a potential agent for diabetes patients with metformin treatment to prevent lactic acidosis and reduce myocardial damages under hypoxic conditions.

• Biomedical Science Letters
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• v.8 no.1
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• pp.21-27
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• 2002

To investigate an effect of bum on the cardiac function, we studied some biochemical assay, ultrastructural changes and stereological analysis in heart tissue. Sprague-Dawley rats were induced a 15% total body surface area scald burn. 5 and 24 hours later, the heart was excised. Burned rats showed the decrease of heart weight per body weight (%) compared with control. The activity of serum aspartate aminotransferase was significantly increased at 5 (p＜0.001) and 24 hours (p＜0.01) after burn compared with control. And the activity of serum LDH was decreased at 5 hours after burn but increased at 24 hours compared with control. Ultrastructurally, enlargement of interstitium and destruction of sarcolemma were observed at 5 and 24 hours after burn. Especially at 5 hours postburn, hypercontraction band was noted and at 24 hours, wavy fiber and muscle fraying were noted. In stereological changes, volume density of mitochondria and myofibril was significantly decreased at postburn 5 and 24 hours. But volume density of sarcoplasmic reticulum was significantly increased at postburn 5 hours. Our data suggest that dermal scald bum causes myocardial dysfunction.

• Biomedical Science Letters
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• v.2 no.1
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• pp.71-90
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• 1996

There is considerable current interest in the effect of regular vigorous exercise and in particular endurance-running as a possible measure in improving myocardial function. Some data indicate that the aging heart may actually suffer from vigorous endurance exercise. On the contrary appropriate exercise in aged animals improves myocardial function and aerobic energy metabolism. So far there is relatively little data to indicate that endurance exercise is in fact beneficial in improving myocardial function or damaging to heart of aged animals. The present investigation aimed to study the possible effect of a long range treadmill training program on the heart in aging rats. Male rats aged 3, 10, and 20 months were divided at random into a control (sedentary) and an exercise group. The training group was exercised for 5 days a week on an automated treadmill for 20minutes at 18m/min over a period of 5 months. The exercise regimen of our experiments did not cause any significant changes in the tissues and ultrastructural as com-pared with sedentary age-matched control. Tissues and ultrastructures of myocardial cells in trained group aged 8 months are intact and well organized as well as sedentary control group. Age associated tissue and ultrastructural changes of trained group aged 15 months included : an increase in transformed mitochondria, vacuoles, lysosomes, lipid droplets and early lipofuscin. But the trained heart did not show significant difference in tissue and ultrastructural properties from those of sedentary controls. Endurance-trained group aged 25 months showed significant qualitative tissue and ultrastructural difference as compared with age-matched controls. In addition to those found in 25 months control group, focal necrosis, myofibril fraying, hypercontraction band, seperation of intercalated discs, degenerating nucleus and infiltration of collagenous fiber into myocyte were noted in trained 25 months group. The stereological examination of the mi-crographs disclosed no significant difference in the myoflbril, mitochondrion, sarcotubule and in-terstitium volume density and surface density of mitochondrial cristae and numerical density of mitochondria between trained and control group aged 8 and 15 months. In the trained 25 months group, significant increase in volume density of interstitium, lipofucsin granule were shown as compared to untrained age-matched control. On the other hand, significant decrease in mitochondrion volume density was shown. The myofibril volume density did not differ between trained and control group although trained group showed slight increase. From the data obtained a reduced mitochondria/myofibrils ratio was found in trained rat heart aged 25 months and there was no difference between trained and control rat aged 15 months. But a slight but not significant increase was found in the trained group aged 8 months as compared with same age control group. Such increase in the ratio in young animals is considered to be of great importance to cardiac pumping and adaptability. Whereas such adaptations don't seem to occur in aged heart muscle. This study proposed that repeated endurance exercise do not cause any significant qualitative and quantitative ultrastructural change of heart muscle in young(3months) and adult (10months) suggesting that the heart is able to adapt to the exercise. On the contrary, the repeated endurance exercise stress may actually induce degenerative changes in the aged heart muscle(20months).