• Journal of Life Science
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• v.19 no.5
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• pp.644-651
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• 2009

The objective of this study was to identify EXE (1 hr a day at 21 m/min for 5 day/wk, at 0 % grade for 6 wk) on myocardium glucose metabolic phenotypic proteins (AMPK-PGC-1${\alpha}$-GLUT-4) and HSP-60 protein expression after ischemia/reperfusion injury (IRI) in STZ-induced rats. EXE was performed using STZ-induced diabetic rats on a rodent treadmill (28 m/min, 1 hr/day, 5 day/wk for 6 wk). The results of this study suggest that i) serum insulin level was not changed among groups (p>l0.05). ii) the LVDP level increased significantly in the STZ-EXE-IRI group compared to the STZ-IRI group at 60 min (p<0.01), 70 min (p<0.05) and 80 min (p<0.05) after reperfusion, respectively, and iii) AMPK phosphorylation (p<0.01), PGC-1${\alpha}$ protein (p<0.001), GLUT-4 protein (p<0.001) and HSP-60 protein expressions (p<0.05) increased significantly in the STZ-EXE-IRI group compared to the STZ-IRI group. In conclusion, the findings of the present study reveal that EXE may provide therapeutic value to insulin dependent diabetic patients with peripheral insulin resistance and myocardium injury by improving glucose metabolic proteins (AMPK-PGC-1${\alpha}$-GLUT-4) and heat shock protein-60 (HSP-60), along with increasing LVDP levels and decreasing glucose levels. Therefore, EXE protects the STZ-induced diabetic myocardium injury against ischemia/ reperfusion injury.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.749-758
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• 1997

Myocardial ischemia-reperfusion injury is known to be mediated by reactive oxygen species. The myocardial cell is equipped with endogenous antioxidant defensive system which can be adaptively stimulated by various oxidative stress. It is postulated that an increased oxygen partial pressure induced by hyperbaric oxygenation impose an oxidative stress on the cells, resulting alterations in the endogenous antioxidant system. In this study we investigated the effect of hyperbaric oxygenation on the activities of myocardial antioxidant enzymes and observed whether the hyperbaric oxygenation could protect the ischemia-reperfusion injury of heart. Rats or rabbits were pretreated with hyperbaric $oxygenation(2{\sim}3\;atm\;O_2/1{\sim}3\;hrs/1{\sim}10\;days)$. The changes in activities of major antioxidant enzymes(superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phasphate dehydrogenase), functional recovery and infarct size were observed in the experimentally induced ischemia-reperfused hearts. In the hearts isolated from rats pretreated with $2\;atm\;O_2/1{\sim}2\;hrs$ for 5 days, the functional recovery after reperfusion(20 min) following global ischemia(25 min) was significantly increased without any observable oxygen toxicity. Lactate dehydrogenase release was also significantly reduced in this hyperbaric oxygenated rat hearts. In in vivo regional ischemia(30 min) model of rabbit hearts, pretreatrment with $2\;atm\;O_2/1\;hr$ for 5 days significantly limited the infarct size. Among the myocardial antioxidant enzymes of rat hearts pretreated with the hyperbaric oxygenation, the activities of catalase, superoxide dismutase and glucose-6-phosphatase dehydrogenase were increased, while those of glutathione peroxidase and reductase were not changed. There were lethal cases in the groups of rats exposed to 3 atm $3\;atm\;O_2/2{\sim}3\;hrs$ for 5 days. A lipid-peroxidation product, rnnlondialdehyde was increased in brains and livers of the rats exposed to$2\;atm\;O_2/2{\sim}3\;hrs/5\;days\;and\;3\;atm\;O_2/1\;hr/5days$. The present results suggest that the pretreatment of hyperbaric oxygenation can protect the post-ischemic rererfused hearts in association with a stimulation of the activities of myocardial antioxidant defensive enzymes, and that the hyperbaric oxygenation of $2\;atm\;O_2/1\;hr$for 5 days would be a safe condition which does not produce any oxygen toxicity.

• Journal of Chest Surgery
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• v.38 no.10 s.255
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• pp.717-720
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• 2005

Here we report a case of posterior left ventricular (LV) free wall rupture following postinfarct ventricular septal rupture (VSR). A 58-year-old man was transferred to the hospital under the impression of acute myocardial infarction. Posterior VSR was seen on echocardiographic examination. The intraaortic balloon pump catheter was introduced percutaneously and the emergent operation was proposed. Sudden circulatory collapse was developed shortly after the anesthetic induction and the patient's chest was hurriedly opened while on cardiopulmonary resuscitation. The acute cardiac tamponade was seen and the blood was seen pumping from the longitudinal tear at the mid-level of LV posterior wall, measuring 2 cm in length. The cardiopulmonary bypass was set and LV reconstruction was done. The postoperative recovery was delayed due to the brain injury presumably caused by preoperative cardiac arrest.

• Journal of Chest Surgery
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• v.30 no.5
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• pp.486-492
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• 1997

We r viewed a policy of primary surgical closure of large ventricular septal defects in small infants. Sixty-three infants met criteria for inclusion in the study, and were divided into two groups based on age: group 1 infants aged less than 5 months(n = 31), and group 2 infants aged 5 months or more(n = 32). Both groups had similar variation in ventricular septal defect location(paramembranous versus muscular), and showed no significant difference in left to right shunt and in ratio of systemic and pulmonary vascualr resistance. Three early deaths(9.7%) occurred in group 1, but no death(0%) in group 2. The causes of death were preoperative cardiac arrest and cerebral injury followed by postoperative respiratory insufficiency in two patients, and preoperative tracheomalacia followed by laryngeal edema and respiratory arrest in one Two patients in group 1 showed postoperative low cardiac output syndrome(6.5% in group 1 versus 0% in group 2). There was no late death during the follow-up per od in both groups. No surviving patients had postoperative patch leakage, or required a second operation. These results indicate that primary surgical closure of large ventricular septal defects, if logical perioperative care is accompanied, can be saefly performed in small infants aged less than 5 months with low postoperative mortality or morbidity rates.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.1-6
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• 1996

We developed an experimental model of brain death using dogs. Brain death was induced by increasing the intracranial pressure (ICP) gradually by continuous Infusion of saline through an epidural Foley catheter in 5 mongrel dogs (weight, 18~22kg). Hemodynamic and electrocardiographic changes were evaluated continuously during the process of brain death and obtained the following results. 1. The average volume and time required to induce brain death was 4.8$\pm$1.0ml and 143.0$\pm$30.9minutes respectively. 2. There was a steady rise of the ICP after starting the constant infusion of saline, and ICP rised continuously until the brain death (122.0$\pm$62.5mmHg). After reaching to the maximal value (125.0$\pm$47.7mmHg) at 30 minutes after brain death, the ICP dropped and remained approximately constant at the slightly higher level than the mean arterial pressure (MAP). 3. MAP showed no change until the establishment of brain death and it declined gradually. The peak heart rate reached to 172.6$\pm$35.3/min at 30 minutes after the brain death. 4. Even though the body temperature and all hemodynamic variables, such as cardiac output, mean pulmonary arterial pressure, left ventricular (LV) end-diastolic pressure and LV maximum + dp/dt, were slightly greater than those of basal state, at the point of brain death, there was no statistically significant change during t e process of brain death. 5. There was no remarkable arrhythmias during the experiment except ventricular premature beats which was observed transiently in one dog at the time of brain death. Hemodynamic changes in the brain death model induced by gradual ICP increment were inconspicuous, and arrhythmias were rarely seen. Hyperdynamic state, which was observed at the point of brain death in another brain death model caused by abrupt ICP increase, was not observed.

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1159-1164
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• 1998

Background: Although operative outcome is progressing due to the development of operative techniques and myocardial protection, some patients face an increased morbidity and mortality. Therefore, it has become increasingly important to predict the operative morbidity and mortality. Material and Method: This retrospective study reports the results of risk factor analysis of morbidity and mortality of 137 consecutive patients who were underwent coronary artery bypass graft surgery(CABG). Preoperative variables were age, sex, preoperative myocardial infarction, operative priority, left ventricular ejection fraction, obesity and triple vessel disease. Postoperative morbidities were arrhythmia, wound infection, cerebral infarction, prolonged postoperative hospitalization, pneumonia, acute renal failure, prolonged use of ventilator and operative death. Result: The mean age of total patients was 56.7 years, from 27 to 74. The overall mortality was 6.6%(9 of 137) with the mortality of 3.9%(5 of 128) for elective operation, and 44.4%(4 of 9) for emergent or urgent cases. The morbidity of patients over 65 years was stastistically higher than that of under 65 years. Sex distribution showed no difference in morbidity, however operative mortality rate was slightly higher in women (5/41, 12.19%) than in men(4/96, 4.17%). Morbidity of emergent or urgent operation was 100%, much higher than that of the elective operation. Mortality of the patients whose left ventricular ejection fraction was under 50% was higher than that of those over 50%. Conclusion: We concluded that the risk factors of morbidity after CABG were old age above 65 years and emergent or urgent operation, and that risk factors of mortality were low left venticular ejection fraction under 50% and emergent or urgent operation.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.2
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• pp.62-70
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• 2015

Purpose: Cardiac complications may occur in cases of organophosphate (OP) poisoning. However, a few studies regarding patterns of cardiac toxicity as determined by transthoracic echocardiography (TTE) after exposure to OP have been reported. In the current study, the authors examined cardiac functions using TTE in patients with myocardial injury caused by exposure to OP. Methods: A retrospective review was conducted on 16 consecutive cases of OP poisoning with myocardial injury (defined as elevated troponin I within 48 hours of arrival at the regional emergency center in South Korea and diagnosed and treated at the center from January 2012 to November 2014. Results: TTE was performed in 11 (69%) of the 16 patients with an elevated troponin I (TnI) level within 48 hours. Of these 11 patients, 5 patients (45.5%) exhibited reduced ejection fraction (EF), and 3 exhibited regional wall motion abnormality (RWMA). Two patients (18.2%) had both reduced systolic function and RWMA. Two of the 5 patients with reduced EF returned to normal systolic function, however two patients did not regain normal systolic function after admission. One patient expired due to multiple organ failure, and 4 patients were transferred with a moribund status. Twelve of 15 patients who survived to discharge (at 4 to 35 months) were followed. Five of these patients died during follow-up and 7 survived without further complications. Conclusion: OP can cause reversible cardiac dysfunction including reduced systolic function and RWMA. Serum TnI may be useful for initial assessment of cardiac function during the workup of patients suffering from OP poisoning. After the initial assessment of cardiac enzyme, further evaluation with TTE in patients with abnormal cardiac enzyme will be necessary to understand the cardiac toxicity.

• Journal of Chest Surgery
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• v.29 no.3
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• pp.255-262
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• 1996

The donor pool for heart transplants is severely limited and there is still a legal problem of brain death. This study assessed the function of hearts "absolute anoxic" for ten minutes after asphyxia by perfusing the hearts on a Langendorfr apparatus for 45 minutes with Krebs-Henseleit buffier at 37 t at 80 cm H2O. Forty isolated rat hearts were divided into four groups. Ten control hearts (group 1) were perfused on the circuit without intervening ischemia. Ten hearts (group 2) were harvested, quickly flushed with 5cc of cold University of Wisconsin solution, and stored in the same cold solution for 4 hours. Ten hearts (group 3) were excised, quickly flushed with 5 u of cold Stanford cardioplegic solution and stored in cold saline solution for 4 hours. Ten asphyxiated hearts (group 4) had warm ischemia for ten minutes and were perfused with 5u of cold Stanford cardioplegia containing 7,500 units of urokinase to dissolve intravascular clots, and stored in cold saline solution for 1.5 hours. Time of spontaneous defibrillation (TSD) after perfusion was significantly longer in group 2, group 3 and group 4 than in group 1. TSD in group 3 and group 4 was significantly longer in comparison to that of group 2. Left ventricular developed pressure(LVDP) at 15 minutes was significantly lower in group 3 and group 4 than in group 1 and group 2. In group 4, LVDP at 30 minutes and 45 minutes was significantly lower compared with that in group 1 . In conclusion, asphyxiated rat hear;ts which had absolute anoxia for 10 minutes after as hyxia showed relatively satisfactory cardiac function. function.

• Applied Microscopy
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• v.27 no.2
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• pp.121-130
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• 1997

It has been demonstrated that majority of cells in the mammalian body such as myocytes and epithelial cells of skin and intestine respond to mechanical force or environmental factors and exhibit partial disruption of cell membrane, i. e., cell wounding, even in a physiological condition. Myocardial cells are rather apt to be wounded than other cells since they are definitely exposed to mechanical stress by contraction-relaxation and blood flow. However, the mechanism how myocardial cells protect themselves against cell wounding is not yet clarified. On this background, the present study was performed to elucidate whether albumin leakage is related to cell wounding and to assess whether diltiazem, a potent calcium channel blocker, is beneficial in isoproterenol-induced cell wounding in the heart. Hearts isolated from New Zealand White rabbits ($1.5\sim2.0kg$ body weight, n=20) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to bolus administration of isoproterenol and diltiazem as following order: $1.6{\mu}M$ isoproterenol at zero min (the beginning point): $16{\mu}M$ diltiazem at 20min; $1.6{\mu}M$ isoproterenol at 25min; $16{\mu}M$ isoproterenol at 45 min; $160{\mu}M$ diltiazem at 65 min; $16{\mu}M$ isoproterenol at 70 min. During all experiments, the left ventricular function was recorded, albumin leakage in the coronary effluents was analyzed by electrophoresis and Western blot, and myocardial cell membranes were examined by conventional transmission electron microscopy. Data were analyzed by t-test and linear regression test. Isoproterenol significantly increased the inotropic and chronotropic contractions, coronary flow, and frequency of arrhythmia, however, diltiazem did not influence on hemodynamics except decrease in the frequency of arrhythmia and a slight decrease in contractility. Isoproterenol also resulted partial disruption of myocardial cell membrane and inclose in albumin leakage, while diltiazem pretreatment showed number of electron-dense plaques in the cell membrane and a tendency of decrease in albumin leakage. These results indicate that albumin leakage may be an indirect index of cell wounding in the heart and diltiazem nay be beneficial to protect myocardial cells against isoproterenol-induced cell wounding. It is likely that diltiazem promotes resealing process of the cell membrane.

• Journal of Life Science
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• v.17 no.4 s.84
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• pp.515-521
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• 2007

Aprotinin, a serine protease inhibitor, has been used to ameliorate the inevitable consequences, including blood component injury after cardiac surgery with cardiopulmonary bypass (CPB). However, there are many arguments on its dosage or usage. We assessed whether administration of low dose of aprotinin in only priming solution has any beneficial effect or reduces its side effects on cardiac surgery. Thirty patients scheduled for elective cardiac surgery were randomly assigned to aprotinin group (n=15) which received aprotinin in priming solution (two million kallikrein inhibitory unit, KIU) and added one million KIU at 1 hour after the beginning of CPB or control group (n=15) which did not receive it. Hematological and biochemical variables, cytokines and cardiac marker levels, and postoperative outcomes were compared between two groups at before, during or after operation. Platelet count in aprotinin group was higher than that of control group at postoperative 24 hr. Activated partial thromboplastin time in aprotinin group was longer than that of control group at intensive care unit (ICU). Troponin-I level and postoperative blood loss volumes in aprotinin group were lower than those of control group at ICU. There were no significant differences between the two groups on the others. These results showed that low dosage of only priming solution during cardiac surgery with CPB reduced platelet destruction and postoperative bleeding, and attenuates myocardial damage. However, further studies need to be carried out with more population or pediatric patients for evaluating various aprotinin usage.