• The Korean Journal of Physiology
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• 제29권1호
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• pp.51-59
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• 1995

This study was designed to test whether or not 1) ischemia-reperfusion attenuates endothelium-dependent relaxation of coronary arteries and 2) preconditioning protects the arterial endothelium from ischemia-reperfusion injury. In anesthetized open chest rabbits, branches of the left circumflex artery were exposed to different combinations of the experimental conditions; ischemia (15 minutes), ischemia (15 minutes)-reperfusion (10 minutes), preconditioning ischemia, and pre-conditioning fellowed by ischemia-reperfusion. Preconditioning consisted of 3 occlusions of 2-min duration, each followed by n 5-min reperfusion. Rings of the artery exposed to the experimental condition and of normal left anterior descending coronary artery were prepared and suspended for isometric force measurement in organ chambers containing Krebs Ringer bicarbonate solution. The rings were contracted with 29.6 mM KCI. Ischemia alone did not attenuate endothelium-dependent relaxation by acetylcholine. However, ischemia-reperfusion significantly impaired endothelium-dependent relaxation. Endothelium-independent relaxation by sodium nitroprusside was not impaired by ischemia-reperfusion and the constrictive response to acetylcholine was not altered in reperfused rings without endothelium, compared with control rings. Arterial rings exposed to preconditioning followed by ischemia-reperfusion exhibited impaired endothelium-dependent relaxation by acetyl-choline. However, although preconditioning not fellowed by ischemia-reperfusion, attenuated endothelium-dependent relaxation at low concentrations of acetylcholine, the magnitude of the impairment by preconditioning followed by ischemia-reperfusion was significantly less than that of the impairment by ischemia-reperfusion alone. These data demonstrate that ischemia-reperfusion significantly attenuates endothelium-dependent relaxation by producing endothelial dysfunction and preconditioning Protects the endothelium of coronary arteries from ischemia-reperfusion injury.

• 한국임상수의학회지
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• 제18권4호
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• pp.402-410
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• 2001

This study was performed to investigate the hemodynamic changes which occur after occlusion of coronary artery and relation to reperfusion arrhythmias(RA) which occur when occlusion materials were removed form coronary artery in dogs. The occlusion of coronary artery was designed by temporary ligation of left circumflex branch of coronary artery during 30 minutes in 16 dogs. During occlusion of coronary artery, cardiac output(CO), mean aortic pressure (mAP), aortic systolic pressure(ASP), aortic diastolic pressure(ADP). left ventricular systolic pressure(LVSP), left ventricular maximum dp/dt (LV max. dp/dt) and left ventricular end-diastolic pressure (LVEDP) were measured. The occurrence of RA were observed for 5 minute after reperfusion by explained of ligation. As a results, cardiac arrest occurred in 4 dogs during occlusion of coronary artery, and RA was not observed in 5 dogs while it was seen in 5 dogs when explained ligation(reperfusion) after 30 minutes, the rest 2 dogs occurred temporary tachycardia. In hemodynamics changes, LVSP decreased by 10.9% and LV max. dp/dt by 5.4 % in comparison to control value which not ligated coronary artery, and LVEDP increased by 73.3%. The CO/min and mAP also decreased by 10.7% and by 11.3% expectedly. In the relationship to occurrence RA and hemodynamics changes, the LVSP and LV max. dp/dt at the time of occlusion in the RA group decreased by 11.9% and 0.8% in comarison to the control value while the decrease was 7.7% and 10% in the non-RA group. But the LVEDP in creased by 109.1% in the RA group while the decreased was 44.6% in the non-RA group. Referring CO/min, the drop was 8.8% in the RA occurrence group and 12.9% in the non-occurence group. These parameters of LVEDP, LV max. dp/dt, and CO were significant difference(p<0.05). The mAP also decreased by 11.9 in the RA group and by 9.8% in the non-RA group, but these defference were not the significant difference.

• Journal of Chest Surgery
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• 제44권4호
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• pp.273-278
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• 2011

Despite aggressive treatment, the mortality rate of cardiogenic shock with acute myocardial infarction (AMI) is high. We performed extracorporeal membrane oxygenation (ECMO) prior to coronary reperfusion, and evaluated the early clinical results and risk factors. Materials and Methods: From May 2006 to November 2009, we reviewed the medical records of 20 patients in cardiogenic shock with AMI (mean age $67.7{\pm}11.7$ yrs, M : F 14 : 6). After initially performing ECMO using the CAPIOX emergency bypass system ($EBS^{(R)}$Terumo, Tokyo, Japan), patients underwent coronary reperfusion (coronary artery bypass grafting, 13; percutaneous coronary intervention, 7). Results: All patients were in a cardiogenic shock state, cardiopulmonary resuscitations (CPR) were performed for fourteen patients (mean CPR time $20.8{\pm}26.0$ min). The mean time from vascular access to the initiation of ECMO was $17.2{\pm}9.4$ min and mean support time was $3.8{\pm}4.0$ days. Fourteen patients were able to be weaned from ECMO and ten patients were discharged (mean admission duration $50.1{\pm}31.6$ days). Patients survived on average $476.6{\pm}374.6$ days of follow-up. Longer CPR and support time, increased cardiac enzyme, lower ejection fraction, lower albumin, and major complications were the risk factors of mortality (p<0.05). Conclusion: The early application of ECMO prior to coronary reperfusion and control of risk factors allowed for good clinical results in cardiogenic shock with AMI.

• Journal of Chest Surgery
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• 제31권9호
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• pp.845-854
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• 1998

Background: S-2-(3 aminoprophlamino) ethylphosphorothioic acid(WR-2721) is one of the radical scavenging thiols. We tested its protective effects in the reperfused heart. Material and Method: The experimental setup was the constant pressure Langendorffs perfusion system. We investigated the radical scavenging properties of this compound in isolated rat hearts which were exposed to 20 minutes ischemia and 20 minutes reperfusion. Four experimental groups were used:group I, control, Amifostine 50 mg(1 mL) peritoneal injection 30 minutes before ischemia(group II), Amifostine 10 mg(0.2 mL) injection during ischemia through coronary artery(group III),and Amifostine 50 mg(1 mL) peritoneal injection 2 hrs before ischemia(group IV). The experimental parameters were the levels of latate, CK-MB, and adenosine deaminase(ADA) in frozen myocardium, the quantity of coronary flow,and left ventricular developed pressure, and it's dp/dt. Statistical analysis was performed using repeated measured analysis of variance and student t-test. Result: The coronary flow of group II and IV were less than group I and III at equilibrium state but recovery of coronary flow at reperfusion state of group II, III, and IV were more increased compared with group I. The change of systolic left ventricular devoloping pressure of group II and IV were less than control group at equilibrium state, which seemed to be the influence of the pharmacological hypotensive effect of amifostine. But it was higher compared with group I at reperfusion state. The lactic acid contents of group II were less than control group in frozen myocardium.(Group I was 0.20 0.29 mM/g vs Group II, which was 0.10 0.11 mM/g). The quantity of CK-MB in myocardial tissue was highest in group IV (P=0.026 I: 120.0 97.8 U/L vs IV: 242.2 79.15 U/L). The adenosine deaminase contents in the coronary flow and frozen myocardium were not significantly different among each group. Conclusion: Amifostine seemed to have significant cardioprotective effect during ischemia and reperfusion injuries of myocardium.

• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.587-595
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• 1999

This study was designed to investigate effects of calcium antagonists on endothelial and neuronal dysfunction of right coronary artery (RCA) induced by ischemia- reperfusion in anesthetized, open-chest pigs. After reperfusion, pigs were sacrificed and the RCA was rapidly dissected for in vitro experiments. Experimental groups were divided into 4 groups: control (C-RCA), ischemia-reperfusion only (I-RCA), verapamil infusion (VI-RCA) and nifedipine infusion (NI-RCA) group, respectively. The ischemia did not affect hemodynamics, mean arterial pressure, heart rate, LVdP/dtmax, and decreased RCA flow. Arterial pressure and heart rate during ischemia-reperfusion were decreased in VI-RCA and NI-RCA, and RCA flow during reperfusion was increased in NI-RCA. 5-Hydroxytryptamine (5-HT) produced concentration-dependent contractions in C-RCA. The 5-HT-induced contractions were potentiated in I-RCA and VI-RCA, but not in NI-RCA. Endothelium-dependent relaxation by calcium ionophore A23187 was inhibited in I-RCA and VI-RCA, and recovered in NI-RCA. Cyclic GMP contents were decreased in I-RCA group alone. Electrical field stimulation in C-RCA produced transient and frequency-dependent contractions and at 50 Hz caused biphasic contractions. The transient contractions were not affected by pretreatment with phentolamine and atropine, but the biphasic contraction was altered by the pretreatment. Both contractions were inhibited in I-RCA, and were partially recovered in VI-RCA and NI-RCA. Ischemia-reperfusion of RCA in pigs causes endothelial and neuronal dysfunctions, and calcium antagonists partially prevent both.

• 한국임상수의학회지
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• 제6권2호
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• pp.269-279
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• 1989

The incidence of reperfusion arrhythmia(RA) according to occlusive position of coronary artery was induced in 25 open-chest dogs anestherized with halothan, these were ligated between anterior ventricular branch and marginal branch of left circumflex artery for 30 minutes and after releasing of the ligation, the incidence of RA was observed during 5 minutes. The incidence rate of RA occurred in 36％(9 heads) of the cases, 20%(5 heads) of them died before reperfusion and 44％(11 heads) of them survived after reperfusion. In the classification according to the length of anterior ventricular branch in left circumflex artery, the incidence rate of RA occurred in 80％ of the group I(5 heads) which belongs to short size of anterior ventricilar branch, in 50% of the group II (8 heads) which belongs to medium size, in 8.3% of the group III(12 heads) which belongs to long size and in 61.5% of the groups I and II(13 heads). These results showed the higher incidence rate of RA than in other occlusive position (left anterior descending artery), and it may be estimated that the incidence of RA changed with the significant difference according to the lengthe of anterior ventricular branch, in other words, dimension of ischemic area in left ventricle.

• Journal of Ginseng Research
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• 제33권4호
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• pp.268-277
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• 2009

Ginsenosides are among the most well-known traditional herbal medicines frequently used for the treatment of cardiovascular symptoms in South Korea. The anti-ischemic effects of compound K (CK), a metabolite of ginsenoside Rb1, on ischemia-induced isolated rat hearts were investigated through the analyses of the changes in the hemodynamics (blood pressure, aortic flow, coronary flow, and cardiac output) and the measurement of the infarct region. The subjects in this study were divided into four groups: the normal control, the CK-alone group, the ischemia-induced group without any treatment, and the ischemia-induced group treated with CK. No significant differences in perfusion pressure, aortic flow, coronary flow, and cardiac output were found between the groups before ischemia was induced. The oxygen and buffer supply was stopped for 30 min to induce ischemia 60 min after reperfusion in the isolated rat hearts, and the CK was administered 5 min before ischemia induction. The CK treatment significantly prevented decreases in perfusion pressure, aortic flow, coronary flow, and cardiac output under ischemic conditions. In addition, the hemodynamics (except for the heart rate) of the group treated with CK significantly recovered 60 min after reperfusion, unlike in the control group. CK significantly limited the infarct. These results suggest that CK treatment has distinct anti-ischemic effects in an exvivo model of an ischemia-reperfusion-induced rat heart.

• Biomolecules & Therapeutics
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• 제7권4호
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• pp.354-361
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• 1999

In this study, the effects of tauroursodeoxycholic acid (TUDCA) on ischemia/ reperfusion injury were investigated on isolated heart perfusion models. Hezrts were perfused with oxygenated Krebs-henseleit solution (pH 7.4, $37^{\cire}C$) on a Langendorff apparatus. After equilibration, isolated hearts were treated with TUDCA 100 and 200 $\mu\textrm{M}$ or vehicle (0.02% DMSO) for 10 min before the onset of ischemia in single treatment group. In 7 day pretreatment group. TUDCA 50, 100 and 200 mg/kg body weight were given orally for 7 days before operation. After global ischemia (30 min), ischemic hearts were reperfused for 30 min. The physiological (i.e. heart rate, left ventricdular developed pressure, coronary flow, double product, time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 810 sec during ischemia, LVDP was 34.0 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 34.3 U/L. Single treatment with TUDCA did not change the postischemic recovery of cardiac function, LDH and time to contractur compared with ischemic control group. TUDCA pretreatment showed the tendency to decrease LDH release and to increase time to contracture and coronary flow. Our findings suggest that TUDCA does not ameliorate ischemia/reperfusion-reduced myocardial damage.

• The Korean Journal of Physiology and Pharmacology
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• 제3권6호
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• pp.579-586
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• 1999

Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg) to I/R hearts in the presence of PMNs $(100{\times}10^6)$ and homologous plasma improved coronary flow and preserved cardiac contractile function (p＜0.001) in comparison to those I/R hearts receiving only vehicle. In addition, C1 INH significantly (p＜0.001) reduced PMN accumulation in the ischemic myocardium as evidenced by an attenuation in myeloperoxidase activity. These findings demonstrate the C1 INH is a potent and effective cardioprotective agent inhibits leukocyte-endothelial interaction and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.

• Journal of Chest Surgery
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• 제28권6호
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• pp.549-556
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• 1995

We investigated the effects of aprotinin, a protease inhibitor, on isolated rat heart subjected to cardioplegia and global ischemia for 4 hours and then reperfused for 40 minutes. Before ischemia, hearts were perfused with either aprotinin 1x105KIU/L[Aprotinin group,n=8 or no aprotinin[control group,n=8 added to Krebs-Henseleite solution for 30 minutes. Hemodynamic and biochemical parameters such as heart rate, LVP, dP/dt, coronary flow and creatine kinase were measured before cardioplegia and after reperfusion 10,20,30,40 minutes. After completion of experiment, wet and dry heart weight were measured for tissue water and water content evaluation. On reperfusion, recovery of LVP of aprotinin group at each time point was significantly better than that of control group[p<0.05 , and of dP/dt at reperfusion 40 minutes[p=0.034 . No statistically significant differences in heart rate, coronary flow and CK were observed between the two groups, but aprotinin group seemed to have better recovery. No significant differences in tissue water and water content were observed between the two group.These results suggest that pretreatment of aprotinin is effective in myocardial preservation in prolonged hypothermic ischemia and reperfusion.