• The Korean Journal of Physiology and Pharmacology
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• v.18 no.5
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• pp.419-423
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• 2014

The purpose of the present study was to investigate cardiac damage biomarkers after a triathlon race in elite and non-elite athlete groups. Fifteen healthy men participated in the study. Based on performance, they were divided into elite athlete group (EG: n＝7) and non-elite athlete group (NEG: n＝8). Participants' blood samples were obtained during four periods: before, immediately, 2 hours and 7 days after finishing the race. creatine kinase (CK), creatine kinase-myoglobin (CK-MB), myoglobin, and lactate dehydrogenase (LDH) were significantly increased in both groups immediately after, and 2 hours after finishing the race (p<.05). CK, CK-MB, and myoglobin were completely recovered after 7 days (p<.05). Hematocrit (Hct) was significantly decreased in both groups (p<.05) 7 days after the race. LDH was significantly decreased in the EG (p<.05) only 7 days after the race. Homoglobin (Hb) was significantly decreased in the NEG (p<.05) only 2 hours after the race. Although cardiac troponin T (cTnT) was significantly increased in the EG but not in the NEG 2hours after the race (p<.05), there was no group-by-time interaction. cTnT was completely recovered in both groups 7 days after the race. In conclusion, cardiac damage occurs during a triathlon race and, is greater in elite than in non-elite. However, all cardiac damage markers return to normal range within 1 week.

• Journal of Korean Medicine for Obesity Research
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• v.17 no.2
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• pp.77-86
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• 2017

Objectives: This study examined the effects of salvianolic acid B (SAB) on exhaustive exercise-induced cardiac muscle damage to rats. Methods: The study was carried out with 12-week-old young adult male Sprague-Dawley rats. Thirty-six rats were divided into 3 groups; normal (n=12), exhaustive exercise group (ExS, n=12) and exhaustive exercise with SAB (ExS+SAB, n=12). Five days before exhaustive exercise, SAB were medicated for 5 days in ExS+SAB group. Rats in ExS and ExS+SAB group were forced to swim for 150 minutes and then they were sacrificed, while rats in normal group were sacrificed at rest. After that, blood was collected and cardiac muscle tissue damage indices were analyzed. Results: Serum aspartate transaminase activity and lactate dehydrogenase activity were significantly lower in ExS+SAB group than in ExS group. Serum creatine phosphokinase activity of ExS+SAB was significantly lower than ExS group. However, the content of serum creatinine had no difference between ExS and ExS+SAB group. In the H&E stained left ventricle myocardium, ExS group showed signs of myocardial damage such as sporadic fragmentation of myocardial fibers, interstitial edema, cytoplasmic eosinophilia and neutrophils infiltration. However, ExS+SAB group alleviated the severity of the signs of myocardial damage. In the myocardial dihydroethidium staining, optical density was remarkably decreased in ExS+SAB group compared to ExS group. Furthermore, the up-regulation of Bax/Bcl-2 ratio was observed in ExS+SAB group compared with ExS group. Conclusions: The above results suggest that SAB may protect cardiac muscle damage via antioxidant activity and prevention of apoptosis.

• Archives of Pharmacal Research
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• v.21 no.5
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• pp.496-502
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• 1998

The present study was carried out to determine the possible use of cTn-I in the cardiac myofibrillar architecture, as a potential target for in vivo radioimmunodetection of cardiac damage in a brain death pig model. Radioiodiantion of the anti-cTn-I 5F4 McAb was carried out by lactoperoxidase method. the percentage iodine incorporation achieved was 70-75%. The radioiodinated McAbs were purified on Sephadex G-25 column and characterised by Paper chromatography, Phast Gel electrophoresis and electroimmunoblotting. Radioiodinated anticTn-I 5F4 McAbs were employed alongside Pyrophosphate($Tc_{99m}$-PPi$) and $Thallium^{201}$ chloride($TI^{201}$) in 24 landrace pigs (brain-dead=18 & sham-operated=6). The percentage cardiac uptake of the radiolabelled antibody injected dose was significantly higher in the brain dead animals(0.196%) as compared to that of sham-operated animals (0.11%). Specific in vivo localization of radiolabelled McAbs in the infarcted cardiac tissue was confirmed by computer-aided reconstruction of 3-D images of the isolated heart. The preliminary results of the study revealed preferential uptake of radiolabelled antibody at the site of myocyte damage resulting from artificially induced brain death.

• Journal of Yeungnam Medical Science
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• v.18 no.1
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• pp.13-29
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• 2001

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First, creatine kinase ME mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins, troponin T (cTnT) and troponin I (cTnI) appeared and displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. The latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone- or together with myoglobin and CK-ME mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For the diagnosis of patient with chest pain, routinely myoglobin and CK-ME mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later and maintained less than 10% in imprecision.

• Proceedings of the Korean Society of Disaster Information Conference
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• 2023.11a
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• pp.129-130
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• 2023

The From COVID-19 until recently, the demand for hiking has been rapidly increasing due to the popularization of mountain seekers.,On weekends and holidays, people who do not hike frequently while hiking in large and small mountains to see wildflowers and foliage in the mountains are more likely to be exposed to safety accidents due to an increase in sudden muscle use.,If you fall or get muscle damage during a hike, you can prevent a major accident with a simple treatment. In some cases, the error of first aid may permanently damage the important function of the body.,In particular, during a safety accident on a mountain, while climbing in light clothes, the body temperature rises due to the sweat that was shed at the beginning, and the blood pressure rises due to the contraction of the blood vessels due to the drop in body temperature from the top, resulting in an emergency such as cardiac arrest.,According to statistics from the National Park Service, nearly half (48%) of deaths in national parks are known to be sudden cardiac deaths.,There are many safety accidents that occur frequently in the mountains, but among them, we will study how to cope with acute diseases such as cardiac arrest due to increased blood pressure due to insufficient body temperature control, chest pain or dyspnea, and heart burden due to excessive hiking.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.6
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• pp.633-641
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• 2017

The aim of this study is to investigate the effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and ER stress of the cardiac muscle in high fat diet-induced obese middle-aged rats. We induced obesity over 6 weeks of period in 40 male Sprague-Dawley rats around 50 weeks old, and were randomly divided into four experimental groups: chow, HFD, exercise+HFD, and exercise+chow. The exercising groups underwent high-intensity intermittent training using a ladder-climbing and weight exercise 3 days/week for a total of 8 weeks. High-fat diet and concurrent exercise resulted in no significant reduction in body weight but caused a significant reduction in visceral fat weight (p<0.05). Expression of $PPAR{\delta}$ increased in the exercise groups and was significantly increased in the high-fat diet+exercise group (p<0.05). Among the ER stress-related proteins, the expression levels of p-PERK and CHOP, related to cardiac muscle damage, were significantly higher in the cardiac muscle of the high-fat diet group (p<0.05), and were significantly reduced by intermittent ladder-climbing exercise training (p<0.05). Specifically, this reduction was greater when the rats underwent exercise after switching back to the chow diet with a reduced caloric intake. Collectively, these results suggest that the combination of intermittent ladder-climbing exercise training and a reduced caloric intake can decrease the levels of ER stress-related proteins that contribute to cardiac muscle damage in obesity and aging. However, additional validation is required to understand the effects of these changes on mitochondrial biogenesis during exercise.

• Journal of Chest Surgery
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• v.16 no.1
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• pp.97-101
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• 1983

The steadily increasing number of operations performed on the heart has given rise to occasional complications involving the nervous system, and this has been interested to cardiac surgeons and neurologists. This survey has been carried out on all Gases submitted to open heart surgery at Seoul National University Hospital during 1982 to determine which operative features were associated with the occurrence of neurological damage. 514 subjects were studied and neurological damage was noted in twenty-five patients [4.9%]. Eight of these 25 patients died in the postoperative period, but neurological damage contributed to the fatal outcome in six cases. Remaining seventeen patients were discharged without problems except one Cortical blindness and one hemiplegic patients who were survived without other problems . A number of features were found to be related to the development of neurological damage, which were age, duration of perfusion, nature of operation, cardiac rhythm and presence of the thrombi or calcification and hypothermic arrest. But many unknown etiological factors are remained out of our sight. A significant increase in the incidence of neurological damage was shown in older age group [13.3% in over 40 year of age], and also the duration of the bypass was associated with subsequent neurological injury especially more than 120 minutes [11.6%]. The presence of atrial fibrillation with intracardiac thrombi or calcification was also a contributing factor to developing neurological complication [16.7%]. These factors were regarded to influence the postoperative neurological complications and more effective method for prevention of these neurologic complication should be studied.

• Herbal Formula Science
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• v.31 no.3
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• pp.157-169
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• 2023

Gracilaria Verrucosa (GV), a seaweed used in traditional Korean medicine, was studied for its effects on MI-induced heart failure in rats. MI is caused by a blocked coronary artery, leading to severe cardiac dysfunction. The study used a rat model to assess cardiac changes over time and evaluate the impact of GV on heart failure. Ischemia was induced through LAD ligation surgery, and the extent of ischemic area was measured as a prognostic factor. GV extract administration significantly improved cardiac morphology and reduced cardiac weight compared to the MI group. GV treatment also improved cardiac function, as evidenced by positive effects on chamber dilation during MI-induced heart failure. Parameters such as ejection fraction (EF) and fractional shortening (FS) were measured. The MI group showed decreased EF and FS compared to the sham group, while these parameters improved in the GV group. GV treatment also reduced levels of LDH, CPK, and CK-MB in the serum, indicating reduced myocardial damage. Histological analysis revealed that GV treatment attenuated cardiac hypertrophy and fibrosis, with reduced collagen deposition in the myocardium. Immunohistochemistry analysis showed suppressed expression of TGF-β1 and collagen 1, involved in fibrosis. In conclusion, GV showed potential in improving cardiac function in a rat model of MI-induced heart failure. It alleviated myocardial damage, attenuated cardiac hypertrophy and fibrosis, and suppressed fibrotic markers. Further studies are needed to explore its clinical efficacy and underlying mechanisms in cardiac diseases beyond animal models.

• The Korean Nurse
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• v.10 no.6 s.56
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• pp.22-25
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• 1971

The recovery of process of brain damage caused by an acute severe cerebral hypoxia has been reported in various literatures. And the possibility of complete recovery of such case was said to be good in younger age group than in adult''s group. We experien

• Korean Circulation Journal
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• v.48 no.11
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• pp.1014-1024
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• 2018

Background and Objectives: Intense exercise (IE) induced myocardial fibrosis (MF) showed contradictory findings in human studies, making the relationship between IE and the development of MF unclear. This study aims to demonstrate exercise induced MF is associated with cardiac damage, and inflammation is essential to the development of exercise induced MF. Methods: Sprague-Dawley rats were submitted to daily 60-minutes treadmill exercise sessions at vigorous or moderate intensity, with 8-, 12-, and 16-week durations; time-matched sedentary rats served as controls. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum cardiac troponin I (cTnI) concentration. After completion of the exercise protocol rats were euthanized. Biventricular morphology, ultrastructure, and collagen deposition were then examined. Protein expression of interleukin $(IL)-1{\beta}$ and monocyte chemotactic protein (MCP)-1 was evaluated in both ventricles. Results: After IE, right but not left ventricle (LV) MF occurred. Serum cTnI levels increased and right ventricular damage was observed at the ultrastructure level in rats that were subjected to long-term IE. Leukocyte infiltration into the right ventricle (RV) rather than LV was observed after long-term IE. Long-term IE also increased protein expression of proinflammation factors including $IL-1{\beta}$ and MCP-1 in the RV. Conclusions: Right ventricular damage induced by long-term IE is pathological and the following inflammatory response is essential to the development of exercise induced MF.