• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.194-194
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• 1996

Pathogenesis of experimental allergic encephalomyelitis was involved with infection, inflammatory reaction, immune reaction etc. We studied on relation of blood vessel system and EAE. So, we measured blood pressure, heart rate and relaxation of isolated blood vessel in control and EAE-induced lewis rats. Blood pressure was decreased before EAE clinical sign (0-20day), but was increased from 23day. In isolated blood vessel, acetylcholine-treated relaxation was different on control, maximum EAE stage, recovery stage. Acetylcholine-treated relaxation was reduced 30% in recovery stage. but, sodium nitroprusside had similar relaxation reaction.

• Archives of Pharmacal Research
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• 제15권1호
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• pp.95-98
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• 1992

Alcoholic extract of seeds of Sesamum indicum (SI, 1-30mg/kg) caused hypotensive action in anesthetized rats. Heart rate was also decreased at slightly higher doses (10-30 mg/kg). Pretreatment with atropine (2 mg/kg) abolished these cardiovascular responses. In isolated spontaneously beating atria from guinea-pigs. SI caused decrease in force and rate of atrial contractions. In isolated guinea-pig ileum and rat uterus, SI (100-1000 ug/ml) produced contractile responses. All these actions of SI were abolished in the presence of atropine ($1\mu$M). These results indicate that alcoholic extract of seeds of Seamum indicum contains acetylcholine-like constituent(s) which explains some of the folkloric uses of plant.

• 대한약리학회지
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• 제22권1호
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• pp.51-59
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• 1986

Lidocaine의 심근수축력 억제 작용에 관한 기전연구 일환으로 lidocaine에 의해 수축력이 감소된 흰쥐 적출심방에 대한 fructose의 효과를 검토하였다. Fructose는 기질제거에 의해 감소된 적출심방의 수축력을 현저히 증가시켰으며, 30mM에서 최대 증가효과를 나타냈다. Krebs-Ringer glucose용액에 현수한 적출심방의 수축력은 0.1mM lidocaine에 의해 약 50%의 감소를 나타냈으며, 30mM fructose의 투여는 이 감소된 수축력을 현저히 증가 시켰다. Lidocaine 억제심방에 대한 fructose의 실험 성적은 pyruvate나 acetate에서 얻은 실험성적과 유사하였다. 그러나 같은 농도의 fructose는 저 calcium(1/2)농도의 Krebs-Ringer glucose medium에서 감소(약 50% 감소)된 적출심방의 수축력을 증가시키지 못하였다. 이상의 결과에서 lidocaine은 심근내 포도당 대사를 해당과정에서 억제한다는 가능성을 재확인하고 있으며, 나아가서 lidocaine은 해당과정의 phosphofructokinase step 이전의 초기단계에서 억제하고 있을 가능성을 시사하고 있다.

• 치과방사선
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• 제27권2호
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• pp.63-81
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• 1997

This study was performed in order to identify changes of the plasma membrane proteins in rat submandibular gland tumors induced by 7,12-dimethylbenz[a]anthracene [DMBA] and X-irradiation. Two kinds of tumor associated membrane proteins (protein A and B) were isolated with 3 M KCl extraction from rat submandibular gland tumors induced by DMBA and X-irradiation. To identify their antigenicities, immunoelectrophoresis and double immunodiffusion was carried out with various proteins extracted from liver, heart, skin and pancreas of adult rats and from embryonic liver, heart and skin. The rabbit antisera against the protein A did not cross-react with any of the proteins extracted from the above mentioned tissues, suggesting that protein A might be tumor specific antigen. However, the rabbit antisera against protein B was precipitated with proteins extracted from the liver of adult and embryonic rats. Polyacrylamide gel electrophoresis of these two proteins (A and B) showed that protein A was a dimer with molecular weights of 69,000 and 35,000 dalton, whereas protein B was a monomer with molecular weight of 50,000 dalton.

• The Korean Journal of Physiology and Pharmacology
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• 제9권2호
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• pp.95-101
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• 2005

In the heart, $Na^{+}-Ca^{2+}$ exchange (NCX) is the major $Ca^{2+}$ extrusion mechanism. NCX has been considered as a relaxation mechanism, as it reduces global $[Ca^{2+}]_i$ raised during activation. However, if NCX locates in the close proximity to the ryanodine receptor, then NCX would curtail $Ca^{2+}$ before its diffusion to global $Ca^{2+}_i$ This will result in a global $[Ca^{2+}]_i$ decrease especially during its ascending phase rather than descending phase. Therefore, NCX would decrease the myocardial contractility rather than inducing relaxation in the heart. This possibility was examined in this study by comparing NCX-induced extrusion of $Ca^{2+}$ after its release from SR in the presence and absence of global $Ca^{2+}_i$ transient in the isolated single rat ventricular myocytes by using patch-clamp technique in a whole-cell configuration. Global $Ca^{2+}_i$ transient was controlled by an internal dialysis with different concentrations of BAPTA added in the pipette. During stimulation with a ramp pulse from +100 mV to -100 mV for 200 ms, global $Ca^{2+}_i$ transient was suppressed only mildly, and completely at 1 mmol/L, and 10 mmol/L BAPTA, respectively. In these situations, ryanodine-sensitive inward NCX current was compared using $100{\mu}mol/L$ ryanodine, $Na^+$ depletion, 5 mmol/L $NaCl_2$ and $1{\mu}mol/L$ nifedipine. Surprisingly, the result showed that the ryanodine-sensitive inward NCX current was well preserved after 10 mmol/L BAPTA to 91 % of that obtained after 1 mmol/L BAPTA. From this result, it is concluded that most of the NCX-induced $Ca^{2+}$ extrusion occurs before the $Ca^{2+}$ diffuses to global $Ca^{2+})i$ in the rat ventricular myocyte.

• BMB Reports
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• 제28권3호
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• pp.254-260
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• 1995

Cytochrome oxidase was purified from bovine-heart mitochondria and its enzymatic properties were examined. The purified cytochrome oxidase was identified by its absorption spectrum and chromatogram through gel filtration. The specific activity, purification degree and yield of purified cytochrome oxidase were 18 nmol/mg/ml/min, 24.83 fold and 0.93%, respectively. The activity of the enzyme assayed by a ferrocytochrome $c-O_2$ system was optimized at $25^{\circ}C$ and pH 6.5. Examining the effect of nonionic detergents established that cytochrome oxidase was deactivated by Triton X-100. The oxidase was activated by Tween 80 and deactivated by Tween 20. The Michaelis constant and maximum velocity of the oxidase for ferrocytochrome c were 0.032~0.044 mM and 0.019~0.021 mM/min, respectively. After adaption to basal diet for a week, experimental diets containing 6 mg Cu/kg, or zero mg Cu/kg, or 12 mg Cu/kg were fed to a control group, a copper-free group and a copper-rich group of Sprague-Dawley rats, respectively, for 4 weeks. The specific activities assayed for the ferrocytochrome $c-O_2$ system of isolated cytochrome oxidase from the rat liver of control, copper-free, and copper-rich group were 1.00, 1.19, and 0.878 nmol/mg/ml/min, respectively. Their degrees of purification were 11.38, 10.82 and 8.78 fold, respectively. The specific activities for liver and heart mitochondrial cytochrome oxidase of copper-free/copper-rich groups assayed using the ferrocytochrome $c-O_2$ system were 81.4% and 96.4%/64.1% and 61.1%, respectively, compared with those of the control.

• 약학회지
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• 제41권6호
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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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• 제22권6호
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• pp.927-935
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• 1989

Using an isolated Rat heart preparation of the Sprague Dawley strain, the YUMC cardioplegic solution k the St. Thomas Hospital Cardioplegic Solution were compared in the non waking K working heart perfusion systems by evaluating the hemodynamics, [bio] chemical, and light microscopic finding The heart rate k coronary flow of the two groups in the 20 minutes post ischemic recovery time were 288.6*6.5 vs 283.7*12 and 21.3*1.0 vs 19.0*1.7 respectively with no statistical significance existing. However the aortic systolic pressure, aortic overflow, cardiac output which were 81.7[4.2 vs 78.4*1.8, 18.3*1.1 vs 13.0*2.5 and 36.9*0.9 vs 32.0*3.2 respectively with P < 0.01 indicate that the comparison of these three parameters is statistically meaningful. The amount of CPK extracted in the 20 minutes post 120 minutes of ischemia was compared for the two cardioplegic solution, the results of which turned out to be similar, light microscopic findings were also found to be similar. It is thought that the YUMC cardioplegic solution provided better results than the St. Thomas hospital solution because of the differing composition of the two solution such as glucose, mannitol, albumin were put only in the former solution enhancing osmolarity of the cardioplegic solution providing better hemodynamic results.

• Journal of Chest Surgery
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• 제33권8호
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• pp.605-612
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• 2000

Background: Ischemic preconditioning enhances the tolerance of myocardium against ischemia/reperfusion injury, with the enhancement of the recovery of post-ischemic myocardial function. This study was disigned to assess whether the protective effect of ischemic preconditioning could provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rate heart. Material and method: Fourty four Spargue-Dawley rats, weighing 300~450gm, were divided into four groups. Group 1(n=7) and group 3(n=12) were subjected to 30 minutes of aerobic Langendorff perfusion without ischemic preconditioning and then preserved in saline solution at 2~4$^{\circ}C$ for 4 hours and 5 respectively. Group 2(n=7) and group 4(n=18) were perfused in the same way for 20 minutes, followed by 3 minutes of global mormothermic ischemia and 10 minutes of perfusion and then preserved in the same cold saline solution for 4 hours and 5 hours respectively. Heart rate, left ventricular developed pressure(LVDP), and coronary flow were measured at 15 minutes during perfusion as baseline. Spontaneous defibrillation time was measured after reperfusion. Heart rate, LVDP, and coronary flow were also recorded at 15 minutes, 30 minutes, and 45 minutes during reperfusion. Samples of the apical left ventricular wall were studied using a transmission electron microscope. Result: Time of spontaneous defibrillation(TSD) was significantly longer in group 4 than in group 1(p<0.001), and TSD in group 1 was significantly longer in comparision to that of group 2(p<0.05). Heart rate at 45 minutes was significantly higher in group 1 than in group 4(p<0.05). Heart rate at 15 min was significantly higher in group 2 than in group 1(p<0.001) and in group 4 than in group 3(p<0.05). Left ventricular developed pressure(LVDP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.01), LVDP at 45 minutes was higher in group 4 than in group 3(p<0.05). Rate-pressure product(RPP) at 30 minutes and 45 minutes was higher in group 1 than in group 4(p<0.05). RPP at 15 minutes was higher in group 2 than in group 1(p<0.01). RPP at 30 minutes and 45 minutes was higher in group 4 than in group 3(p<0.05). Group 2 showed relatively less sarcoplasmic edema and less nuclear chromatin clearance than group 1. Group 4 showed less myocardial cell damage than group 3, group 4 showed less myocardial cell damage than group 3, group 4 showed more myocardial cell edema than group 1. Conclusion: Ischemic preconditioning enhanced the recovery of postischemic myocardial function after 4 hours and 5 hours preservation. However, it was not demonstrated that ischemic preconditioning could definitely provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rat heart.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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• pp.705-714
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• 1998

Cerebral blood vessels relax when extracellular $K^+$ concentrations $([K^+])_e$ are elevated moderately $(2{\sim}15$ mM, $K^+-induced$ vasorelaxation). We have therefore studied the underlying mechanism for this $K^+-induced$ vasorelaxation in the isolated middle cerebral arteries (MCAs). The effects of ouabain and $Ba^{2+}\;on\;K^+-induced$ vasorelaxation were examined to determine the role of sodium pump and/or Ba-sensitive process (possibly, inward rectifier K current) in the mechanism. Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans MCAs $(216{\pm}3\;{\mu}m,\;347{\pm}7\;{\mu}m,\;and\;597{\pm}39\;{\mu}m$ in diameter when stretched to a tension equivalent to 55 mmHg). High $K^+$ (125 mM) and $PGF_{2{\alpha}}\;(1{\sim}10\;{\mu}M)$ induced concentration-dependent contractions in all 3 species, while histamine $(10{\sim}50\;{\mu}M)$ evoked contraction only in the rabbits and induced relaxation in the rats and humans. Addition of $K^+\;(2{\sim}10\;{\mu}M)$ to the control solution induced vasorelaxations. These effects were inhibited by the pretreatment with both ouabain $(10\;{\mu}M)$ and $Ba^{2+}\;(0.1{\sim}0.3\;mM)$ in the rat, but only with ouabain $(10\;{\mu}M)$ in the rabbit and human. These results suggest that $K^+-induced$ vasorelaxation occurs via the stimulation of electrogenic Na pump in the rabbit and human MCAs, while in the rat MCAs via the activation of both Na pump and Ba-sensitive process.