• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2003년도 생물공학의 동향(XII)
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• pp.95-97
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• 2003

본 연구에서는 손상된 심근의 재생을 위하여 골수단핵세포를 SD 래트에 이식하였고 5주 후에 심근의 재생, 신생혈관의 형성과 더불어 심장의 기능이 향상되었음을 확인할 수 있었다. 골수단핵세포를 손상된 심근경색 부위에 넣어주는 것은 추가 보완 실험을 통하여 심근경색의 치료법으로서 이용될 수 있을 것이다.

• Journal of Chest Surgery
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• 제33권8호
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• pp.613-622
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• 2000

Background: The aim of this study is to define the cardioprotective effects(functional and metabolic) of newly developed DelNido cardioplegic solution(containing plasma solution, mannitol, magnesium and lidocaine). Material and Method: This study assessed the function of rat hearts after itermittent infusion of DelNido cardioplegia with different preserving methods(Air or Icebox) for 2hours and perfusing the hearts on a Langendorff apparatus. Heart rate, left ventricular developed pressure(LVDP) and coronary flow, were measured at pre-ischemic, post-reperfusion 15min, 30min and 45min. Coronary flow was standardized to dry heart weight. Each weight was weighted to calculate water content. Creatine kinase-MB isoenzyme release was measured and ultrastructural assessment was done with electron microscopes. Result: DelNido group was better than St, Thomas group and Icebox group was better than Room-air group. Conclusion: DelNido cardioplegia have better myocardial protective effects than St. Thomas cardioplegia when they were preserved in the Room-air. But we can not tell the difference between Delnido cardiplegia with Air preserving method and St. Thomas cardioplegia with Icebox.

• Journal of Chest Surgery
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• 제13권4호
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• pp.338-345
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• 1980

We have modified an isolated perfusion rat heart model of cardiopulmonary bypass, with which we are able to screen the effects of various cardioplegic solutions and hypothermia upon the ability of the heart to survivie during and recover from period of ischemic arrest. The modified experimental model was differed from the original as follow : a heat coil chamber of atrial and aortic reservoir provided temperature control, and the perfusate was gassed with each pure oxygen and pure carbon dioxide in 95:5 ratio. The Langendorff perfusion was initiated for a 10 minute period by introducing perfusate at $37^{\circ}C.$ into the aorta from the aortic reservoir located 100 cm above the heart. The isolated perfused working rat heart model was a left heart preparation in which oxygenated perfusion medium (at $37^{\circ}C.$) entered the cannulated left atrium at a pressure of 20 cm $H_{2}O$ and was passed to the ventricle, from which it was sponeously elected(no electrical pacing) via an aortic cannula, against a hydrostatic pressure of 100cm $H_{2}O$. during this working period various indices of cardiac functin were measured. The cardiac functions were stable for over 3 hour with perfusion of Krebs-Henseleit bicarbonate buffer solution containing only glucose (11.1 mM/L). The percentage of cardiac functins were maintained about 94% on heart rate, 80.6% on peak aortic pressure, 87.7% on coronary flow and 76.3% on aortic flow rate after 3 hour of working heart perfusion at a pressure of 20 cm $H_{2}O$. We believe this preparation to be a good biochemical model for the human heart which offers many advantages including economic, speed of preparation, reproducibility, and the ability to handle large numbers.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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• pp.753-761
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• 1998

Preconditioning of a heart with small doses of catecholamines induces a tolerance against the subsequent lethal ischemia. The present study was performed to find a specific receptor pathway involved with the catecholamine preconditioning and to test if adenosine plays a role in this cardioprotective effect. Isolated rat hearts, pretreated with small doses of ${\alpha}-\;or\;{\beta}-adrenergic$ agonists/antagonists, were subjected to 20 minutes ischemia and 20 minutes reperfusion by Langendorff perfusion method. Cardiac mechanical functions, lactate dehydrogenase and adenosine release from the hearts were measured before and after the drug treatments and ischemia. In another series of experiments, adenosine $A_1\;or\;A_2$ receptor blockers were treated prior to administration of adrenergic agonists. Pretreatments of a ${\beta}-agonist,\;isoproterenol(10^{-9}{\sim}10^{-7}\;M)$ markedly improved the post-ischemic mechanical function and reduced the lactate dehydrogenase release. Similar cardioprotective effect was observed with an ?-agonist, phenylephrine pretreatment, but much higher $concentration(10^{-4}\;M)$ was needed to achieve the same degree of cardioprotection. The cardioprotective effects of isoproterenol and phenylephrine pretreatments were blocked by a ${\beta}_1-adrenergic$ receptor antagonist, atenolol, but not by an ${\alpha}_1-antagonist,$ prazosin. Adenosine release from the heart was increased by isoproterenol, and the increase was also blocked by atenolol, but not by prazosin. A selective $A_1-adenosine$ receptor antagonist, 1,3-dipropyl-8-cyclopentyl xanthine (DPCPX) blocked the cardioprotection by isoproterenol pretreatment. These results suggest that catecholamine pretreatment protects rat myocardium against ischemia and reperfusion injury by mediation of ${\beta}_1-adrenergic$ receptor pathway, and that adenosine is involved in this cardioprotective effect.

• The Korean Journal of Physiology and Pharmacology
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• 제18권6호
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• pp.481-487
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• 2014

Ischemic postconditioning (IPost) could decrease ischemia-reperfusion (IR) injury. It has not yet reported whether IPost is useful when ischemic heart disease is accompanied with co-morbidities like hyperthyroidism. The aim of this study was to examine the effect of IPost on myocardial IR injury in hyperthyroid male rats. Hyperthyroidism was induced with administration of thyroxine in drinking water (12 mg/L) over a period of 21 days. After thoracotomy, the hearts of control and hyperthyroid rats were perfused in the Langendorff apparatus and subjected to 30 minutes global ischemia, followed by 120 minutes reperfusion; IPost, intermittent early reperfusion, was induced instantly following ischemia. In control rats, IPost significantly improved the left ventricular developed pressure (LVDP) and ${\pm}dp/dt$ during reperfusion (p<0.05); however it had no effect in hyperthyroid rats. In addition, hyperthyroidism significantly increased basal $NO_x$ (nitrate+nitrite) content in serum ($125.5{\pm}5.4{\mu}mol/L$ vs. $102.8{\pm}3.7{\mu}mol/L$; p<0.05) and heart ($34.9{\pm}4.1{\mu}mol/L$ vs. $19.9{\pm}1.94{\mu}mol/L$; p<0.05). In hyperthyroid groups, heart $NO_x$ concentration significantly increased after IR and IPost, whereas in the control groups, heart $NO_x$ were significantly higher after IR and lower after IPost (p<0.05). IPost reduced infarct size (p<0.05) only in control groups. In hyperthyroid group subjected to IPost, aminoguanidine, an inducible nitric oxide (NO) inhibitor, significantly reduced both the infarct size and heart $NO_x$ concentrations. In conclusion, unlike normal rats, IPost cycles following reperfusion does not provide cardioprotection against IR injury in hyperthyroid rats; an effect that may be due to NO overproduction because it is restored by iNOS inhibition.

• Journal of Ginseng Research
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• 제31권1호
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• pp.23-33
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• 2007

Ginsenosides are one of the most well-known traditional herbal medicines frequently used for the treatment of cardiovascular symptoms in korea. The anti-ischemic effects of the mixture of ginsenoside $Rg_3$, and CK on ischemia-induced isolated rat heart were investigated through analyses of changes in hemodynamics ; blood pressure, aortic flow, coronary flow, and cardiac output. The subjects in this study were divided into four groups: normal control, the mixture of ginsenoside $Rg_3$ and CK, an ischemia-induced group without any treatment, and an ischemia-induced group treated with the mixture of ginsenoside $Rg_3$ and CK. There were no significant differences in perfusion pressure, aortic flow, coronary flow and cardiac output between them before ischemia was induced. The supply of oxygen and buffer was stopped for five minutes to induce ischemia in isolated rat hearts, and the mixture of ginsenoside $Rg_3$ and CK was administered during ischemia induction. Treatments of the mixture of ginsenoside $Rg_3$ and CK significantly prevented decreases in perfusion pressure, aortic flow, coronary flow, and cardiac output under ischemic conditions. In addition, hemodynamics (except heart rate) of the group treated with the mixture of ginsenoside $Rg_3$ and CK significantly recovered 60 minutes after reperfusion compared to the control group (mixture+ischemia vs ischemia - average perfusion pressure: 74.4${\pm}$2.97% vs. 85.1${\pm}$3.01%, average aortic flow volume: 49.11${\pm}$2.72% vs. 59.97${\pm}$2.93%, average coronary flow volume: 58.50${\pm}$2.81% vs. 72.72${\pm}$2.99%, and average cardiac output: 52.47${\pm}$2.78% vs. 63.11${\pm}$2.76%, p<0.01, respectively). These results suggest that treatment of the mixture of ginsenoside $Rg_3$ and CK has distinct anti-ischemic effects in ex vivo model of ischemia-induced rat heart.

• Applied Microscopy
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• 제20권1호
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• pp.65-76
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• 1990

The effect of calcium-free reperfusion for 5, 10, and 15 minutes, respectively, followed by continuous reperfusion with normal Tyrode solution containing 1.0mM calcium chloride, after global ischemia in the isolated perfused guinea pig heart by Langendorff techniques was examined with transmission electron microscope. Compared to the nomal Tyrode solution-perfused control hearts, the 5 minute calcium-free-reperfused hearts showed loss or thickening of Z lines, focal sarcolemmal disruption, mitochondrial swelling, clumping of chroma-tin, intracellular fluid accumulation, and some separation of cell junctions, especially the fasciae adherentes. These changes became more severe in the hearts of 10 minute calcium-free reperfusion. Subsarcolemmal larger bleb and near complete separation of cell junctions were noticed. In the 15 minute calcium-free-reperfused hearts, irreversible ultrastructural changes including contraction bands, biazrre mitochondria, and sarcolemmal destruction were widely distributed. The severity of myocardial changes were in accordance with the duration of calcium-free reperfusion. These changes indicate that calcium-free reperfusion regardless of its duration could not salvage the post-ischemic myocardium probably due to development of calcium paradox.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1998년도 Proceedings of UNESCO-internetwork Cooperative Regional Seminar and Workshop on Bioassay Guided Isolation of Bioactive Substances from Natural Products and Microbial Products
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• pp.199-199
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• 1998

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on retrograded aortic perfusion model. Hearts from Sprague-Dawley rats were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, 37) on a Langendorff apparatus. After equilibration, hearts were treated with ursodeoxycholic acid 10, 20, 40 and 800 M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. Following 25 min of global ischemia, ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular diastolic pressure, coronary flow and time to contracture formation) and biochemical (lactate dehydrogenase, LDH) endpoints were evaluated. In vehicle group, time to contracture formation (TTC) value was 19.5 min during ischemia, LVDP was 20.8 mmHg at the endpoint of reperfusion and LDH activity in reperfusate was 59.7 U/L. Cardioprotective effects of UDCA following ischemia/reperfusion consisted of a reduced TTC (EC$\_$25/ = 16.10 M), reduced LDH release and enhanced recovery of contractile function during reperfusion. Especially, the treatments of UDCA 80 M remarkably increased LVDP (68.1 mmHg) and reduced LDH release (33.2 U/L). Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage, in agreement with physiological and biochemical parameters.

• 약학회지
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• 제27권2호
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• pp.155-161
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• 1983

The rates of deterioration of contractile forces of isolated hearts from ginseng component treated rats were determined. Rat papillary muscles were also used to study the influence of ginseng on the mechanical performance of heart. Rats weighing 200-300g were administered orally with ginseng ethanol extract (100mg/kg/day), ginseng total saponin (50mg/kg/day) and ginsenoside Rbl (5mg/kg/ day) for a week respectively. The isolated hearts from rats were perfused with Krebs-Henseleit solution by Langendorff perfusion apparatus. The force-velocity relation was clearly seen with the load-generator equipped isotonic shortening recording apparatus. The control group was only able to maintain 60% of their initial contractile forces after 120 minutes of perfusion, whereas ginseng ethanol extract treated group was able to sustain nearly their initial strength even after 120 minutes of perfusion. The similar effects were seen in the hearts treated with total ginseng saponin and ginsenoside Rb$_{1}$. Ginseng ethanol extract did alter mechanical performance of rat ventricular myocardium. It increased both maximum velocity(Vmax) of isotonic shortening and isometric force (P$_{0}$) and showed increased velocity of shortening significantly (P<0,05) at any one afterload.d.

• 대한한방소아과학회지
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• 제24권3호
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• pp.106-120
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• 2010

Objectives: Sanjointang has been clinically used much for treating sleeplessness. However, the effects of Sanjointang in artificial sleep deprivation situations are not known. The purpose of this study is to evaluate the heart rate, left ventricular systolic pressure, left ventricular diastolic pressure, +dp/dt maximum, -dp/dt maximum, and -dp/dt / +dp/dt ratio which are related to the hemodynamic functions of the heart by using sleep-deprived Sparague-Dawley rats, in order to clarify the impact of Sanjointang on hemodynamic functions of the heart of sleep deprived rats. Methods: Eighteen hearts were removed from the male Sparague-Dawley rats weighting about 180g were perfused by the Langendorff technique with modified 37 Krebs-Henseleit's buffer solution at a constant perfusion pressure (60mmHg). They were randomly assigned to one of the following three groups, 1) Normal group (those which did not have sleep deprivation and received normal saline administration), 2) Control group (sleep deprived and normal saline administered), 3) Sample group (sleep deprived and Sanjointang was administered). Control and sample groups rats were deprived 96 hours of sleep by using the modified multiple platform technique. Heart rate, left ventricular systolic pressure, left ventricular diastolic pressure, +dp/dt maximum, -dp/dt maximum, -dp/dt / +dp/dt ratio were evaluated at baseline after the administration of either normal saline or Sanjointang. Results: The heart rate and -dp/dt / +dp/dt ratio was significantly decreased in rats with 96 hours of sleep deprived significantly decreased. The change in the heart rate after administering Sanjointang did not show any significant difference. The left ventricular systolic pressure of the removed heart significantly decreased due to Sanjointang administration, while the left ventricular diastolic pressure significantly increased (p<0.05). The +dp/dt maximum and -dp/dt maximum both significantly decreased in the removed heart after administering Sanjointang. (p<0.05). There was no significant difference observed in the -dp/dt / +dp/dt ratio after administering Sanjointang. Conclusions: According to the results above, sleep deprivation significantly decreases heart rate and -dp/dt / +dp/dt ratio. This is considered as a result of exhaustion due to accumulation of fatigue. Meanwhile, Sanjointang reduced left ventricular systolic pressure and raised left ventricular diastolic pressure, and relieved the contractility and relaxation of the myocardium. Consequently, this reduces the burden of the heart and creates a relatively stabilized heart condition similar to a sleeping condition.