• Korean Journal of Veterinary Research
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• v.29 no.4
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• pp.461-467
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• 1989

The activity of lactate dehydrogenase in plasma and various tissues(skeletal muscle, cardiac muscle, liver, lung, kidney and spleen) of Korean native cattle in a Chonju abattoir, the Breeding Stock Farm and Animal Farm of Chonbuk University was determined by using ultra violet method. Using polyacrylamide gel electrophoresis, the lactate dehydrogenase isoenzyme distrimution of plasma and various tissues in Korean native cattle was studied. The plasma lactate dehydrogenase activity of Korean native cattle was $554.80{\pm}92.70IU/l$ and the lactate dehydrogenase activity of male plasma was $543.96{\pm}97.89IU/l$, which was lower than that of female plasma, $579.19{\pm}78.09IU/l$. The plasma lactate dehydrogenase activity of calf was $557.31{\pm}110.27IU/l$ and was no significantly different from that of adult Korean native cattle. But the range of calf lactate dehydrogenase activity was larger than that of adult Korean native cattle. In tissues, the lactate dehydrogenase activity was decreased in order of lung, kidney, spleen, liver, heart and skeletal muscle. The lung had the greatest activity and the skeletal muscle had the least. Lactate dehydrogenase isoenzymes in plasma and tissues were found to have a characteristic distribution and quantitative isoenzyme patterns. In plasma, the LDH1 usually had the greatest activity and other isoenzymes showed a decreasing tendency in order of LDH2, LDH3, LDH4 and LDH5. The distribution of lactate dehydrogenase isoenzymes had a wide variation in tissues. But the distribution of LDH isoenzymes in plasma was similar to that in kidney, and also cardiac muscle and spleen had similar pattern in LDH isoenzymes distribution.

• Preventive Nutrition and Food Science
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• v.6 no.1
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• pp.43-50
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• 2001

The effects of cardiac ischemia-reperfusion and $\beta$-adrenergic stimulation on metabolic function and energetics were investigated in Lan gendorff-perfused spontaneously hypertensive rat (SHR) hearts. Sarcoplasmic reticulum {TEX}$Ca^{2+}${/TEX}-dependent ATPase and cardiac lactate dehydrogenase (LDH) are additionally studied. The perfusion medium (1.0 mM {TEX}$Ca^{2+}${/TEX}) contained 5 mM glucose(+5 U/L insulin) and 2 mM pyruvate as substrates. Global ischemia was induced by reducing perfusion pressure of 100 to 40 cm {TEX}$H_{2}${/TEX}O, followed by 20 min reperfusin. Isoproterenol (ISO, 1$\mu$M) was infused for 10 min. Coronary vascular resistance and myocardial oxygen consumption ({TEX}$MVO_{2}${/TEX}) of SHR were increased in parallel with enhanced venous lactate during ischemia and reperfusion compared to those of Sprague Dawley (SD) hearts. Although ischemia-induced increase in venous lactate and combined adenosine plus inosine was abolished, coronary vasodilation produced in SD during reperfusion. In SHR, depressed reactive hyperemia was associated with a fall in cardiac ATP and CrP/Pi ratio and a rise in intracellular lactate/Pyruvate ratio. On the other hand, ISO produced coronary functional hyperemia and an increase in {TEX}$MVO_{2}${/TEX}. However, these responses were less than those in SHR hearts. The ATPase activity of SHR was attenuated in free {TEX}$Ca^{2+}${/TEX} concentrations used under basal condition and with ISO compared to that of SD. Venous lactate output and cardiac LDH activity were augmented in SHR as influenced by ISO. These results demonstrate that coronary reactive and functional hyperemia was dpressed in SHR, which cold be explained by alterations in the cytosolic phosphorylation potential and the cytosolic redox state manipulated by LDH, and by abnormal free calcium handling.

• BMB Reports
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• v.36 no.6
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• pp.593-596
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• 2003

The effects of $N{\omega}$-nitro-L-arginine methylester (L-NAME) and L-arginine on cardiotoxicity that is induced by doxorubicin (Dox) were investigated. A single dose of Dox 15 mg/kg i.p. induced cardiotoxicity, manifested biochemically by a significant elevation of serum creatine phosphokinase (CPK) activity [EC 2.7.3.2]. Moreover, cardiotoxicity was further confirmed by a significant increase in lipid peroxides, measured as malon-di-aldehyde (MDA) in cardiac tissue homogenates. The administration of L-NAME 4 mg/kg/d p.o. in drinking water 5 days before and 3 days after the Dox injection significantly ameliorated the cardiotoxic effects of Dox, judged by the improvement in both serum CPK activity and lipid peroxides in the cardiac tissue homogenates. On the other hand, the administration of L-arginine 70 mg/kg/d p.o. did not protect the cardiac tissues against the toxicity that was induced by the Dox treatment. The findings of this study suggest that L-NAME can attenuate the cardiac dysfunction that is produced by the Dox treatment via the mechanism(s), which may involve the inhibition of the nitric oxide (NO) formation. L-NAME may, therefore, be a beneficial remedy for cardiotoxicity that is induced by Dox and can then be used to improve the therapeutic index of Dox.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.43-50
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• 2004

Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in a marked cardiac contractile dysfunction. Amrinone, a specific inhibitor of phosphodiesterase 3, has an antioxidant activity against PMNs. Therefore, we hypothesized that amrinone could attenuate PMNs-Induced cardiac dysfunction by suppression of reactive oxygen species (ROS) produced fby PMNs. In the present study, we examined the effects of amrinone on isolated ischemic (20 min) and reperfused (45 min) rat hearts perfused with PMNs. Amrinone at $25\;{\mu}M$, given to hearts during the first 5 min of reperfusion, significantly improved coronary flow, left ventricular developed pressure (P<0.001), and the maximal rate of development of left ventricular developed pressure (P<0.001), compared with ischemic/reperfused hearts perfused with PMNs in the absence of amrinone. In addition, amrinone significantly reduced myeloperoxidase activity by 50.8%, indicating decreased PMNs infiltration (p< 0.001). Superoxide radical and hydrogen peroxide production were also significantly reduced in fMLP- and PMA-stimulated PMNs pretreated with amrinone. Hydroxyl radical was scavenged by amrinone. fMLP-induced elevation of $[Ca^{2+}]_i$ was also inhibited by amrinone. These results provide evidence that amrinone can significantly attenuate PMN-induced cardiac contractile dysfunction in the ischemic/reperfused rat heart via attenuation of PMNs infiltration into the myocardium and suppression of ROS release by PMNs.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.3
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• pp.229-229
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• 2019

• Fire Science and Engineering
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• v.27 no.6
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• pp.122-128
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• 2013

This study analyzed the emergency activity daily reports and emergency instruction sheets of the research subjects and proceeded with the shockable cardiac arrest cases transported to 119 emergency units for two years before the hospital from January 1, 2010 through December 31, 2011. The most frequently predicted instruction by the dispatchers at the 119 Emergency Situation Control Center was 74 cases of fainting (33.3%). Among varied types of predicted instructions, 112 cases (50.5%) like fainting, chest pain, general prostration and others were not able to be predicted while predictable instructions involved with cardiac arrest such as consciousness disorders, difficult breathing, cardiac attacks and convulsion were 110 cases (49.5%). In such cases, success rates of cardiopulmonary resuscitation (CPR) trials by eyewitnesses at predictable instructions involved with cardiac arrests were significantly higher. As mentioned, situation agents must categorize types of cardiac arrests accurately by posing questions over assessments regarding patients' consciousness and respiration in detail. The patients categorized by such methods must guide eyewitnesses to be able to do CPR. Moreover, not only emergency medical technicians who receive predictable instructions involved with cardiac arrests given by dispatchers (49.5%) but also filed emergency medical technicians who are not able to reach a precise conclusion to non-cardiac arrests on unpredictable instructions on cardiac arrests (50.5%) must prepare for situations related to cardiac arrests before being dispatched to the field.

• Journal of Life Science
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• v.15 no.1 s.68
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• pp.80-86
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• 2005

To achieve the purpose of this study, forty-eight male Sprague-Dawley rats were assigned to control and three endurance exercise group. 36 rats were forced to exercise according to exercise intensity for 8 weeks and 12 rats were untrained for control group. Cardiac cytosol was extracted from cardiac tissue and cardiac mitochondria was purified from the cytosol. Purified mitochondria were separated into four fraction: inner membrane, outer membrane inter membrane space and matrix. The changes of cytosolic and mitochondrial LDH isozymes activity were measure. Relative activity $(\%)$ of cytosol for low and control group showed the following order of prevalence $AB_3>A_2B_2>B_4>A_3B>A_4$ for moderate and high group : $AB_3>B_4>A_2B_2>A_3B>A_4$. Outer membrane for low group showed $AB_3>B_4>A_2B_2$, for moderate group:$ B_4>AB_3>A_2B_2$, for high and control group: $B_4>A_3B$. Inter membrane space for low, moderate and high group showed $B_4>AB_3>A_2B_2>A_3B>A_4$, for control group: $B_4>A_3B>AB_3>A_2B_2>A_4$. Inner membrane for all group showed $B_4>AB_3>A_2B_2>A_3B>A_4$. Matrix for control, low, moderate and high group showed $B_4>AB_3>A_2B_2>A_3B>A_4$. These results suggest that long term exercise intensity effect on cardiac tissue cytosolic and mitochondrial activity and $A_4,\;A_3B,\;A_2B_2,\;AB_3\;and\;B_4$ isozymes were found entirely in mitochondrial fraction.

• Journal of Satellite, Information and Communications
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• v.9 no.1
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• pp.85-89
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• 2014

Electrocardiogram (ECG) is a diagnostic test which records the electrical activity of the heart, shows abnormal rhythms and detects heart muscle damages. With this ECG signal, medical centers diagnose patients' heart disease symptoms. A normal resting heart rate for adults rages from 60 to 100 beats a minute. An irregular heartbeat is called "arrhythmia", and arrhythmia is also called "cardiac dysrhythmia". In an arrhythmia, the heartbeat maybe too slow(slower than 60beats), too rapid(faster than 100beats), too irregular, etc. Among these symptoms of arrhythmia, if the heart beat is slower than the normal range, the symptom is called "bradycardia", and if it is faster than the range, it is called "tachycardia" In this letters, we proposed the detection algorithm of cardiac arrhythmia in ECG signal using R-R interval through the detection of R-peak.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.482-489
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• 2020

G protein-coupled receptor kinase 5 (GRK5) has been considered as a potential target for the treatment of heart failure as it has been reported to be an important regulator of pathological cardiac hypertrophy. To discover novel scaffolds that selectively inhibit GRK5, we have identified a novel small molecule inhibitor of GRK5, KR-39038 [7-((3-((4-((3-aminopropyl)amino)butyl)amino)propyl)amino)-2-(2-chlorophenyl)-6-fluoroquinazolin-4(3H)-one]. KR-39038 exhibited potent inhibitory activity (IC₅₀ value=0.02 µM) against GRK5 and significantly inhibited angiotensin II-induced cellular hypertrophy and HDAC5 phosphorylation in neonatal cardiomyocytes. In the pressure overload-induced cardiac hypertrophy mouse model, the daily oral administration of KR-39038 (30 mg/kg) for 14 days showed a 43% reduction in the left ventricular weight. Besides, KR-39038 treatment (10 and 30 mg/kg/day, p.o.) showed significant preservation of cardiac function and attenuation of myocardial remodeling in a rat model of chronic heart failure following coronary artery ligation. These results suggest that potent GRK5 inhibitor could effectively attenuate both cardiac hypertrophy and dysfunction in experimental heart failure, and KR-39038 may be useful as an effective GRK5 inhibitor for pharmaceutical applications.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.4
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• pp.335-344
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• 2024

Diphenyleneiodonium (DPI) has been widely used as an inhibitor of NADPH oxidase (Nox) to discover its function in cardiac myocytes under various stimuli. However, the effects of DPI itself on Ca²⁺ signaling and contraction in cardiac myocytes under control conditions have not been understood. We investigated the effects of DPI on contraction and Ca²⁺ signaling and their underlying mechanisms using video edge detection, confocal imaging, and whole-cell patch clamp technique in isolated rat cardiac myocytes. Application of DPI suppressed cell shortenings in a concentration-dependent manner (IC₅₀ of ≅0.17 µM) with a maximal inhibition of ~70% at ~100 µM. DPI decreased the magnitude of Ca²⁺ transient and sarcoplasmic reticulum Ca²⁺ content by 20%-30% at 3 µM that is usually used to remove the Nox activity, with no effect on fractional release. There was no significant change in the half-decay time of Ca²⁺ transients by DPI. The L-type Ca²⁺ current (I_Ca) was decreased concentration-dependently by DPI (IC₅₀ of ≅40.3 µM) with ≅13.1%-inhibition at 3 µM. The frequency of Ca²⁺ sparks was reduced by 3 µM DPI (by ~25%), which was resistant to a brief removal of external Ca²⁺ and Na⁺. Mitochondrial superoxide level was reduced by DPI at 3-100 µM. Our data suggest that DPI may suppress L-type Ca²⁺ channel and RyR, thereby attenuating Ca²⁺-induced Ca²⁺ release and contractility in cardiac myocytes, and that such DPI effects may be related to mitochondrial metabolic suppression.