• Journal of Biomedical Engineering Research
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• v.15 no.4
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• pp.407-412
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• 1994

This paper describes the construction of an anisotropic three dimensional ventricular model based on the bidomain model. The cardiac activation process in the normal cardiac cell and the myocardial ischemic cell are simulated by the Huygen's principle. The depolarization process in the myocardial ischemia displays the delayed activation compared to the normal state. The repolarization process is simulated by the myocardial potential at the arbitrary ellapsed time after activation process. Using the potential data, the equivalent cardiac source at the arbitrary time can be computed. In conclusion, this simulation suggests the possibilities of the depolarization and the repolarization process in the normal and abnormal myocardiac cells.

• Proceedings of the KOSOMBE Conference
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• v.1994 no.12
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• pp.61-64
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• 1994

This paper describes the construction of an anisotropic three dimensional ventricular model based on the bidomain model. The cardiac artivation process in the normal cardiac cell and the myocardiac ischemic cell are simulated by the Huygen's principle. The depolarization process in the myocardial ischemia displays the delayed activation compared to the normal state. The repolarization process is simulated by the myocardial potential at the arbitrary ellapsed time after activation process.

• Journal of Chest Surgery
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• v.21 no.2
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• pp.231-239
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• 1988

Currently numerous methods are in use for myocardial hypothermia as a myocardial preservation modality for cardiac operation. During cardiac ischemia after crystalloid cardioplegia[4C GIK solution], topical cold saline[Group I, a=9], topical ice slush[Group II, n=9] and topical ice chip[Group III, a=10] have been compared for myocardial surface cooling in the isolated rat heart model of cardiopulmonary bypass. During postischemic period, hemodynamic functions[aortic flow, coronary flow, peak aortic pressure and heart rate], biochemical enzymatic activities and cellular injuries with electron microscope were evaluated in this isolated rat heart perfusion model. Postischemic aortic flow, cardiac output and peak aortic pressure in Group I and Group II recovered better than Group III.[p< 0.05] Postischemic creatine kinase and lactate dehydrogenase leakages in Group II and Group III increased more than Group l and postischemic mitochondrial swelling in Group III was more severe than Group I, and Group II.[p< 0.05] These results suggest that topical cold saline was the better method than topical ice slush or topical ice chip as a myocardial preservation modality in the isolated rat heart model of cardiopulmonary bypass.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.6
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• pp.515-523
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• 2000

Polymorphonuclear leukocytes (PMNs) play an important role in myocardial ischemia/reperfusion (MI/R) injury. Moreover, platelets are also important blood cells that can aggravate myocardial ischemic injury. This study was designed to test the effects of PMNs and platelets separately and together in provoking cardiac dysfunction in isolated perfused rat hearts following ischemia and reperfusion. Additional control rat hearts were perfused with $75{\times}10^6$ PMNs, with $75{\times}10^6$ platelets, or with $75{\times}10^6\;PMNs+75{\times}10^6$ platelets over a five minute perfusion followed by a 75 min observation period. No significant reduction in coronary flow (CF), left ventricular developed pressure (LVDP), or the first derivative of LVDP (dP/dt max) was observed at the end of the observation period in any non-ischemic group. Similarly, global ischemia (I) for 20 min followed by 45 minutes of reperfusion (R) produced no sustained effects on the final recovery of any of these parameters in any group of hearts perfused in the absence of blood cells. However, I/R hearts perfused with either PMNs or platelets alone exhibited decreases in these variables of $5{\sim}10%$ (p＜0.05 from control). Furthermore, I/R hearts perfused with both PMNs and platelets exhibited decreases of 50 to 60% in all measurements of cardiac function (p＜0.01). These dual cell perfused I/R hearts also exhibited marked increases in cardiac myeloperoxidase (MPO) activity indicating a significant PMN infiltration, and enhanced P-selectin expression on the coronary microvascular endothelium. All cardiaodynamic effects as well as PMN accumulation and P-selectin expression were markedly attenuated by a recombinant soluble PSGL-1 which inhibits selectin mediated cell adhesion. These results provide evidence that platelets and PMNs act synergistically in provoking post-reperfusion cardiac dysfunction, and that this may be largely due to cell to cell interactions mediated by P-selectin. These results also demonstrate that a recombinant soluble PSGL-1 reduces myocardial reperfusion injury by platelet and PMNs interaction.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.4
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• pp.283-289
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• 2013

This study was designed to evaluate the protective effect of Korean red ginseng (KRG) against ischemia/reperfusion (I/R) injury in isolated guinea pig heart. KRG has been shown to possess various ginsenosides, which are the major components of Panax ginseng. These components are known naturally occurring compounds with beneficial effects and free radical scavenging activity. The heart was induced to ischemia for 60 min, followed by 120 min reperfusion. The hearts were randomly allocated into five groups (n=8 for each group): normal control (N/C), KRG control, I/R control, 250 mg/kg KRG group and 500 mg/kg KRG group. KRG significantly increased hemodynamics parameters such as aortic flow, coronary flow and cardiac output. Moreover, KRG significantly increased left ventricular systolic pressure (LVSP), the maximal rate of contraction (+dP/$dt_{max}$) and maximal rate of relaxation (-dP/$dt_{max}$). Also, treatment of KRG ameliorated electrocardiographic index such as the QRS, QT and RR intervals. Moreover, KRG significantly suppressed the lactate dehydrogenase, creatine kinase-MB fraction and cardiac troponin I and ameliorated the oxidative stress markers such as malondialdehyde and glutathione. KRG was standardized through ultra performance liquid chromatograph analysis for its major ginsenosides. Taken together, KRG has been shown to prevent cardiac injury by normalizing the biochemical and oxidative stress.

• YAKHAK HOEJI
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• v.41 no.6
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• pp.829-836
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• 1997

Studies on the effect of quinones on cardiac function has been conducted with normal hearts. But not with injured hearts, I.e. ischemia/reperfusion-injured heart. Quinone compounds are known to produce oxygen free radicals during metabolism, and for this reason, quinones are implicated in the aggravation of ischemia/reperfusion injury or cardioprotection, as in the case of ischemic preconditioning depending on the experimental conditions. The present study was carried out to examine the effect of 2-chloro-3-(4-cyanophenylamino)-1.4-naphthoquinone (NQ-Y15) on cardiac function of ischemic/reperfused and normal rat hearts. In isolated perfused hearts, various functional parameters such as left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (EDP) and maximum positive and negative dP/dt ($[\pm}dP/dt_{max}$), time to contracture, heart rate (HR) and coronary flow rate (CFR) were measured before and 30 min after dosing and following 25 min ischemia/30min reperfusion. NQ-Y15 increased LVDP, +dP/$d_{max}$and -dP/$dt_{min}$ by 18%. 30%, and 40%, respectively. There were no significant changes in other haemodynamic parameters. After ischemia/reperfusion injury, pretreatment with NQ-Y15 induced a significant decrease in LVDP and $[\pm}dP/dt_{max}$, but an increase in EDP. LDH-release was not significantly increased. These results suggested that NQ-Y15 may augment the ventricular contractility but it makes hearts more vulnerable to ischemia/reperfusion injury.

• Journal of Chest Surgery
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• v.24 no.4
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• pp.331-337
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• 1991

Recent experimental work indicates latamoxef sodium used as a broadspectrum antibiotics generates oxygen-free radicals. The present study represents an attempt to investigate whether reperfusate containing Shiomarin[85% latamoxef sodium+15% mannitol] might decrease the post-ischemic recovery of cardiac function. In the investigation, twelve isolated rat hearts were subjected to 270 minutes of cold total global ischemia. After the cold total global ischemia, six hearts[KHB group] were reperfused with Krebs-Henseleit buffer solution and the other six hearts[LMS group] with Krebs-Henseleit buffer solution containing latamoxef sodium[200ug /L]. Postischemic recovery rate of heart rate, aortic systolic pressure, aortic flow, coronary flow and cardiac output at 20 minutes reperfusion was 100.66$\pm$10.38, 85.25$\pm$7.61, 78.95$\pm$6. 02, 78.85$\pm$8.86 and 79.11$\pm$6.54 percent respectively in the KHB group and 97.96$\pm$4.19, 87. 72$\pm$4.37, 81.74$\pm$6.80, 82.69$\pm$10.01 and 81.90$\pm$6.67 percent respectively in the LMS group. The hemodynamic data revealed no significant difference in the post-ischemic recovery rate of the two groups. This finding suggests that reperfusate containing Shiomarin[latamoxef sodium, 200ug /L] does not affect the cardiac functional recovery after cold total global ischemia.

• 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.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.479-484
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• 1999

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

• 대한핵의학회:학술대회논문집
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• 2006.05a
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• pp.51-52
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• 2006