• Journal of Chest Surgery
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• v.27 no.6
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• pp.427-434
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• 1994

A clinical study was designed to evaluate myocardial metabolism during continuous cold blood cardioplegia [Group A, n=10] in comparison with continuous warm blood cardioplegia [Group B, n=10], in a prospective randomized manner. Myocardial metabolism was assessed in two ways: either by collecting blood from coronary sinus before and after cardiopulmonary bypass or by collecting blood from cardioplegic affluent and effluent simultaneously at the beginning and at the end of cardioplegia. The former samples were assayed for gas analysis, lactic acid and cardiac enzyme [CK, LDH, SGOT] and the latter for gas analysis and lactic acid as a maker of anaerobic metabolism. The results were as follows. 1] Myocardial metabolism was shown to be continued in the state of cardioplegia at lower temperature as evidenced by high oxygen extraction of cardioplegic solution in Group A. 2] Anaerobic metabolism occurring at lower temperature in spite of continuous cold blood cardioplegia can be significantly reduced by continuous perfusion of normothermic blood cardioplegics as evidenced by significant reduction of lactate production in Group B [p〈0.05]. 3] Better myocardial protection can be achieved by employing continuous warm blood cardioplegia as evidenced by less cardiac enzyme release in Group B after cardiopulmonary bypass.

• Journal of Nutrition and Health
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• v.25 no.7
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• pp.597-607
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• 1992

The present study examined effects of caffeine on coronary circulation myocardial oxygen me-tabolism and calcium release in isolated perfused guinea pig hearts. Intracoronary caffeine({{{{ {10 }^{-5 } }}}}∼{{{{ { 10}^{-3 } }}}}M) was employed for 10 minutes to measure coronary perfusate flow(CF) and coronary vascular sresistance(CVR) at a constant coronary perfusion pressure of 80 cmH2O Perfusate myocardial oxygen consumption(MVO2) and percent oxygen extraction(%EC2) were calcula-ted. In addition calcium contents in both perfusate samples were measured to calculate calcium release in coronary venous effluent. Caffeine significantly decreased CF and increased CVR during 10 minutes of caffeine perfusion regardless of dose of caffeine perfused exhibiting time-response. While % EO2 was significantly enhanced with caffeine MVO2 was markedly reduced. The coronary venous perfusate pH dcreased during the perfusion with caffeine. These changes were consistent with caffeine-induced metabolic acidosis. Calcium release appeared to be dose-dependent and high dose of caffeine greatly increased venous calcium release even 2 minutes after perfusion with carffeine. These finding in dicate that caffeine produced coronary vasoconst-riction with increased calcium release in isolated perfused guinea pig hearts. Additionaly this vasoconstrictor response mignt be due tin part to the direct actions of caffeine.

• Journal of Nutrition and Health
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• v.28 no.2
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• pp.115-126
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• 1995

The effects of energy-yielding substrates on coronary circulation, myocardial oxygen metabolism, and intramyocytic adenylates of perfused Wistar control rat(WC) and spontaneously hypertensive rat(SHR) hearts were examined under basal and $\beta$-adrenergic stimulation conditions. The perfusion medium (1.0mM Ca2+) contained 5mM glucose (+5U/l insulin) in combination with 5mM pyruvate, 5mM lacate, 5mM acetate, or 5mM octanoate as energy substrates. Hearts were perfused with each substrate buffer for 20min under basal conditions. Coronary functinal hyperemia was induced by infusing for 20min isoproterenol (ISO, 1uM), a $\beta$-receptor agonist. Cardiac adenylates, glycolytic intermediates, and coronary venous lactate were measured by using an enzymatic analysis technique. Under basal conditions, acetate and octanoate significantly increased coronary flow(CF) of WC in parallel with myocardial oxygen consumption. However, CF of SHR was partly attenuated by coronary vasoconstriction despite metabolic acidosis. In addition, pyruvate and lactate depressd ISO-induced coronary functional hyperemia in SHR. It should be noted that octanoate exhibited coronary dysfunction under ISO conditions. On the other hand, fat substrates depleted myocardial high energy phosphate pool and accumulated breakdown intermediates. In SHR with coronary vasoconstriction under basal conditions, and with depressed coronary functional hyperemia, high energy phosphates were greatly depleted. These results suggest that energy substrates in the myocardium and coronary smooth muscle alter remarkably coronary circulation, and that coronary circulatory function is associated with a reserve of high energy phosphates and a balance between breakdown and nono synthesis of energy phosphates. These findings could be explained by alterations in the cytosolic redox state manipulated by LDH and hence in the cytosolic phosphorylation potential, which might be involved in hypertension of SHR.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.3
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• pp.209-217
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• 2024

In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague-Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.

• Journal of Ginseng Research
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• v.43 no.4
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• pp.517-526
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• 2019

Background: The root of Panax ginseng, a member of Araliaceae family, has been used as herbal medicine and functional food in Asia for thousands of years. According to Traditional Chinese medicine, ginseng is the most widely used "Qi-invigorating" herbs, which provides tonic and preventive effects by resisting oxidative stress, influencing energy metabolism, and improving mitochondrial function. Very few reports have systematically measured cell mitochondrial bioenergetics after ginseng treatment. Methods: Here, H9C2 cell line, a rat cardiomyoblast, was treated with ginseng extracts having extracted using solvents of different polarity, i.e., water, 50% ethanol, and 90% ethanol, and subsequently, the oxygen consumption rate in healthy and tert-butyl hydroperoxideetreated live cultures was determined by Seahorse extracellular flux analyzer. Results: The 90% ethanol extracts of ginseng possessed the strongest antioxidative and tonic activities to mitochondrial respiration and therefore provided the best protective effects to H9C2 cardiomyocytes. By increasing the spare respiratory capacity of stressed H9C2 cells up to three-folds of that of healthy cells, the 90% ethanol extracts of ginseng greatly improved the tolerance of myocardial cells to oxidative damage. Conclusion: These results demonstrated that the low polarity extracts of ginseng could be the best extract, as compared with others, in regulating the oxygen consumption rate of cultured cardiomyocytes during mitochondrial respiration.

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.61-69
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• 1983

Hypothermia is an essential preparatory procedure for cardiac surgery, which lows the metabolic rate and myocardial oxygen demand. However, hypothermia itself is a stress enough to change the tonus of sympathoadrenal system, especially the cardiovascular responses to the catecholamines. It is reported that the positive chronotropic and inotropic response of catecholamines is exaggerated during hypothermia because of decreased norepinephrine uptake at the junctional cleft or decreased catecholamine metabolism. On the other hand, there are evidences of diminished catecholamines responses in low temperature ana further, interconversion of adrenergic receptors is also suggested. Present investigation was planned to observe the cardiovascular changes and its responses to catecholamines during surface hypothermia in cat. Healthy mongrel cats, weighing $2{\sim}3\;kg$, anesthetized with secobarbital(30 mg/kg), were permitted to hypothermia by external cooling technic. Esophageal temperature, ECG (lead II), heart rate, left ventricular pressure with dP/dt, carotid artery pressure and left ventricular contractile force were monitored with Polygragh (Model 7, Grass), and the respiration was maintained with artificial respirator (V 5 KG, Narco). Followings are summarized results. 1) Surface cooling caused progressive decrease of body temperature and reached $l8.8{\pm}0.8^{\circ}C$ and $16.9{\pm}0.6^{\circ}C$ in 120 and 150 min respectively, after immersion into ice water, and ventricular fibrillation was developed at $20.4{\pm}0.65^{\circ}C$. 2) Heart rate, blood pressure and myocardial contractility were decreased after initial increase as the body temperature falls. 3) Systolic and diastolicdd P/dt of left ventricular pressure were decreased and that the decrement of diastolic dP/dt was more marked. 4) On ECG, ST depression, Twave inversion and prolongation of PR interval were prominent in hypothermia, and moreover, the prolongation of PR interval was marked just prior to the development of ventricular fibrillation. 5) The cardiovascular responses to catecholamines, especially to isoproterenol, were suppressed under hypothermia.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.109-118
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• 1991

The present study was conducted to assess the possible contribution of arachidonic acid to generation of reactive oxygen metabolites and myocardial damage in ischemic-reperfused heart. Langendorff preparations of isolated rat heart were made ischemic by hypoperfusion (0.5 ml/min) for 45 min, and then followed by normal oxygenated reperfusion (7 ml/min). The generation of superoxide anion was estimated by measuring the SOD-inhibitable ferricytochrome C reduction. The myocardial cellular damage was observed by measuring LDH released into the coronary effluent. Oxygenated reperfusion following a period of ischemia produced superoxide anion, which was inhibited by both indomethacin (60 nmole/ml) and ibuprofen $(30\;{\mu}g/ml)$. Sodium arachidonate $(10^{-7}-10^{-2}{\mu}g/ml)$ administered during the period of oxygenated reperfusion stimulated superoxide anion production dose-dependently. The rate of arachidonate-induced superoxide generation was markedly inhibited by indomethacin, a cyclooxygenase inhibitor; nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, and by eicosatetraynoic acid (ETYA), a substrate inhibitor of arachidonic acid metabolism. The release of LDH was increased by Na arachidonate and was inhibited by superoxide dismutase. The release of LDH induced by arachidonic acid was also inhibited by indomethacin, NDGA and ETYA. In conclusion, the present result suggests that arachidonic acid metabolism is involved in the production of reactive oxygen metabolite and plays a contributory role in the genesis of reperfusion injuy of myocardium.

• The Korean Journal of Nuclear Medicine Technology
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• v.22 no.2
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• pp.74-78
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• 2018

Purpose $[^{11}C]$acetate has been proved useful in detecting the myocardial oxygen metabolism and various malignancies including prostate cancer, hepatocellular carcinoma, renal cell carcinoma and brain tumors. The purpose of study was to improve the radiosynthesis yield of $[^{11}C]$acetate on a automated radiosynthesis module. Materials and Methods $[^{11}C]$acetate was prepared by carboxylation of grignard reagent, methylmagnesium chloride, with $[^{11}C]$$CO_2$ gas, followed by hydrolysis with 1 mM acetic acid and purification using solid phase extraction cartridges. The effect of the reaction temperature ($0^{\circ}C$, $10^{\circ}C$, $-55^{\circ}C$) and cyclotron beam time (10 min, 15 min, 20 min, 25 min) on the radiosynthesis yield were investigated in the $[^{11}C]$acetate labeling reaction. Results The maximum radiosynthesis yield was obtained at $-10^{\circ}C$ of reaction temperature. The radioactivities of $[^{11}C]$acetate acquired at $-10^{\circ}C$ reaction temperature was 2.4 times higher than those of $[^{11}C]$acetate acquired at $-55^{\circ}C$. Radiosynthesis yield of $[^{11}C]$acetate increased with increasing cyclotron beam time. Conclusion This study shows that radiosynthesis yield of $[^{11}C]$acetate highly dependent on reaction temperature. The best radiosynthesis yield was obtained in reaction of grignard reagent with $[^{11}C]$$CO_2$ at $-10^{\circ}C$. This radiolabeling conditions will be ideal for routine clinical application.