• The Journal of Pediatrics of Korean Medicine
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• v.14 no.2
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• pp.1-32
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• 2000

It has long been known that SOAT is effective for sudden palpitation occurring unexpectedly in Oriental Medicine. However, effect of SOAT on the isolated heart has not been studied yet. The purpose of this study is to investigate the effect of SOAT on hemodynamics and ECG of isolated rat hearts induced by electrical stimulation using Langendorff perfusion apparatus for nonworking heart. SOAT extract was manufactured by water-alcohol precipitated method. Sprague-Dawley rats weighting $120{\sim}150g$ were used for the experiments, Subject animals were divided into four groups, which are consisted of 1) control(Group orally administered by normal saline 1ml for 14days), 2) sample A(Group orally administered by SOAT extract 1ml for 14days), 3) sample C(Group injected by SOAT extract 0.5ml after stimulation, 4) sample C(Group injected by SOAT extract 1ml after stimulation. To evluate the effects of SOAT on hemodynamics and ECG of isolated rat heart induced by stimulation, heart rate, left ventricular pressure, systolic power, diastolic power, coronary artery perfusion volume and ECG were measured using Langendorff apparatus in both stimulation mode(5 volts, 450 beats/min) and arrythmic mode(5 volts, 420 beats/min including 60 beats/min) The results obtained are as follows : 1. After receiving stressful electrical stimuli, isolated heart showed the heart rate, left ventricular pressure, systolic power, diastolic power, coronary artery perfusion volume were all decreased temporarily, but perfusion continued longer recovery to the control state appeared. However, the coronary artery perfusion volume diminished continuously. 2. The heart rates did not change significantly with both stimulation mode and arrhythmic mode, among experimental groups. 3. The left ventricular pressure showed with both stimulation mode and arrhythmic mode, the significant changes(p<0.05) especially in the injection sample group. In case of stimulation mode, low concentration injection group(0.5ml) was more significantly increased rather than high concentration group(1ml) and in case of arrhythmic mode, high density group(1ml) was so increased than the other(0.5ml). 4. For the systolic power and diastolic power, no significant changes were noticed in the stimulation mode, but in the arrhythmic mode of injection sample groups, significant change(p<0.05) was noticed in both systolic power and diastolic power. Specially the high concentration group(1ml) showed more significant increase than the low concentration group. 5. For the coronary artery perfusion volume, no significant change difference among sample groups was observed in both the stimulation mode and the arrhythmic mode. 6. For the ECG recordings, arrhythmia was induced by electrical stimulus of arrythmia mode and after the stimulus was removed, irregular wave appeared temporarily, but as perpusion continued, recovery to the control state was abtained like the stimulation mode. According to the above results, SOAT significantly changed the hemodynamic data from the electrically stressed, isolated hearts of connected Langendorff perfusion apparatus and we propose SOAT has the direct effects on the muscular function of heart.

• YAKHAK HOEJI
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• v.31 no.3
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• pp.140-148
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• 1987

The effects of orally administered ginseng ethanol extract on the calcium release from sarcoplasmic reticulum (SR) calcium pool and on the calcium content in the rat heart perfused with the Langendorff apparatus. The total amount of calcium released from SR calcium pool and the total calcium content in the rat heart were significantly decreased by 43% and 26%, respectively compared with the control.

• The Journal of Korean Medicine
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• v.18 no.2
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• pp.340-354
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• 1997

Background : The stenosis of the coronary artery results in a decrease in the myocardial oxygen supply, ischemia and infarction. Jakamchotang as a drug of liquid is generally regarded to have the effect of arrythmia, palpitation from Heart disease and promoting the flow of Ki and Blood. Methods : The purpose of this experimental study is to find whether Jakamchotang is effective or not in curing ischemia in isolated perfused rat hearts and to measure the degree of its curing effect. In this study, under the Langendorff apparatus, ischemia was induced in isolated Sprague-Dawley rat hearts by ceasing the perfusion for 20 minites. Subjects were divided into a normal saline orally administered group(control group), an Jakamchotang orally 100mg administered group (sample A), an Jakamchotang orally 300mg administered group (sample B), and an Jakamchotang injection perfused group(sample C). The heart rates, left ventricular pressure, myocardial dilatation/contraction, cardiac perfusion flow and cardiac ezyme(LDH, CPK) of the four group were measured and compared in order to assess the influence of Jakamchotang on isolated perfused rat hearts recovering abillity from ischemia and infarction. results : 1. Heart rates were increased significantly in Jakamchotang orally 100mg administered group, Jakamchotang orally 300mg administered group and Jakamchotang injection perfused group on perfusion and reperfusion(p<0.01). 2. Left ventricular pressure were increased significantly in Jakamchotang orally 100mg administered group and 300mg administered and Jakamchotang injection perfused group(p<0.01) in comparison with control group on perfusion, but every group did not significant on reperfusion. 3. While there were no differances in each group's abillities of myocardial dilatation, the ability of myocardial constriction of Jakamchotang 100mg administered group only on perfusion was significantly greater than that of control group(p<0.05). 4. CBF was no significant on perfusion and reperfusion in comparison with control group(N.S.) 5. LDH was not significantly decreased on perfusion, but significactly decreased in Jakamchotang orally 100mg administered group, Jakamchotang orally 300mg administered group on reperfusion. 6. CPK was significantly decreased in Jakamchotang orally 100mg administered group, 300mg administered and Jakamchotang injection perfused group on perfusion(p<0.01), but was not significantly in Jakamchotang 300mg administered group only on reperfusion(P<0.05) Conclusion : According to the result above, Jakamchotang have an effect to recover in the isolated perfused rat hearts. Especially, the effect of Jakamchotang in orally adminstered group is greater than that of Jakamchotang injection perfused group on preischemia. The followings are the two important results of this study: First, the effect of Jakamchotang used traditionally on heart disease was proved statistcally under the Langendorff apparatus. Second, on the basis of this study, the effect of other type medications on myocardial ischemia can be evaluted in further studies.

• Journal of Chest Surgery
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• v.21 no.2
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• pp.246-253
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• 1988

An in vitro model providing with a recirculating perfusion apparatus using an isolated canine heart and its autogenous blood, which was prepared for study of myocardial protection method. This apparatus was easily used by quick connect system and maintained well heart function for about 2 hours. The Langendorff perfusion was initiated for a 10 minute period by introducing perfusate at 37` into the aorta from aortic reservoir located 100 cm above the heart. The isolated perfused working canine heart model was a left heart preparation in which oxygenated perfusion medium [at 37K] entered the cannulated left atrium at a constant flow rate [900ml/ min] under 20 mmHg overflow system and was spontaneously ejected[no electrical pacing] via an cannula against a hydrostatic pressure of 80 cm H2O. During this working period, various indices of cardiac function were measured. The cardiac functions were stable for over 2 hours with perfusion of Krebs-Henseleit solution and autologous blood[1:1] mixture in volume and maintained heart rate ]]3-122/bpm peak systolic pressure 109-113 mmHg, cardiac output 900 ml / min and left atrial mean pressure 8-9 mmHg. In this model, the efficiency of myocardia] protection could be easily measured by means of functional, enzymatic, biochemical and ultrastructural assessment. And also, we believe this model to be a useful assessment screening model of recovery state after long duration of myocardial preservation of donor heart without difficult transplantation procedures.

• YAKHAK HOEJI
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• v.27 no.2
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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.

• Journal of Chest Surgery
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• v.33 no.8
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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.

• Archives of Pharmacal Research
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• v.8 no.2
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• pp.49-57
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• 1985

The effect of ginseng components on the potassium depleted cardiomyopathic rat heart was investigated. In the perfused heart experiment using Langendorff apparatus, the deterioration rate of contriactile force of potassium depleted rat heart (low potassium diet group) was faster than that of normal rat heart and ginseng components showed the ability to slow the deterioration rate of potassium depleted hearts. Both sialic acid contents in carcolemmal ghost and sialyltransferase activity of 40,000 * g subcellular fraction prepared from cardiac ventricular tissue of low potassium diet group were significantly decreased compared to those of normal group. The decrease of the sialic acid content and sialyltransferase activity in sarcolemma of low potassium diet group was inhibited when ginseng was concomitantly administered. Calcium uptake of sarcoplasmic reticulum prepared from low potassium diet group was significantly greaterthan that of normal group. Ginseng extract or total saponin showed the tendency to inhibit the increase of cacium uptake.

• Biomolecules & Therapeutics
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• v.7 no.4
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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.

• Journal of Chest Surgery
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• v.23 no.6
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• pp.1074-1083
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• 1990

This study was evaluated the metabolic, physiologic and histologic effects of myocardial protection of verapamil[isoveratril]on isolated rat hearts to 90 minutes of ischemic arrest. Heart was perfused with a modified Kreb’s Henseleit bicarbonate buffer with glucose and arrested with retrograde coronary perfusion by glucose insulin[GI], potassium and verapamil. Mean aortic systolic pressure, heart rate, coronary flows were measured and morphologic changes were examined during working heart perfusion. Perfusion and arrest were controlled four groups subjected 60 isolated rat hearts. Four groups hearts reperfused during 40 minutes after 90 minutes global ischemia for physiologic recovery. 15 hearts of four groups were assayed to histological morphologic changes. GI treated hearts recovered less than 28% of function and changed more than 80% of mitochondria of control group. Verapamil hearts[0.2, 0.1 gm/kg] recovered more than 88% of function and permitted the maintenance of continuous cellular level of Serum Glutamic Oxalaxetate Transaminase[SGOT], but declined 28% of Phosphate Kinase[CP], GI treated heart showed widespread evidence of extensive damage of mitochondria. The damage was that interstitial huge edema are present and there was contraction band formation within the swollen cells. The verapamil and potassium group were not found morphologic change compared with control group. Their functions were shown that metabolic and physiologic action of verapamil-group lasted 20 minutes longer than potassium group.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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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.