• Korean Journal of Veterinary Research
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• v.39 no.1
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• pp.62-69
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• 1999

Although it has been reported that hormones or chemicals, which increase in intracellular cAMP, produced $Mg^{2+}$ release from the heart, it is not well characterized whether a specific $Mg^{2+}$ exchanger is involved in cAMP-induced $Mg^{2+}$ efflux in the mammalian hearts. In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on $Mg^{2+}$ regulation in the perfused rat heart and isolated myocytes. The $Mg^{2+}$ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes induced a $Mg^{2+}$ efflux in the dose dependent manners. $Mg^{2+}$ efflux was stimulated by cAMP modulators (forskolin, IBMX and Ro20-1724) in the perfused hearts and myocytes. cAMP-induced $Mg^{2+}$ efflux was inhibited by $H_7$, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant $Mg^{2+}$ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of $Mg^{2+}$ efflux in the hearts may be involved in ion transport system ($Na^+-Ca^{2+}$ and $Na^+-Mg^{2+}$ exchanger).

• Journal of Chest Surgery
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• v.25 no.2
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• pp.125-130
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• 1992

To evaluate the effect of oxygenation[95% O2+5% CO2] of St. Thomas Hospital No.2 cardioplegic solution[Plegisol], 20 isolated perfused rat hearts were studied under hyp-othermic[20oC] ischemic arrest for 2 hours with infusion of cardioplegic solution every 30 minutes throughout the ischemic period. Ten isolated hearts were studied with the oxygenated cardioplegic solution and 10 another isolated hearts with the nonoxygenated one. Mean oxygen tensions of the nonoxygenated and oxygenated cardioplegic solutions were 150mmHg and 470mmHg, respectively. Two in 10 hearts infused with the nonaxygenated cardioplegic solution were not recovered from nonworking heart due to persistent ventricular fibrillation. In comparing hem-odynamic parameters between both groups, the mean postischemic recovery[expressed as a percentage of its preischemic control value] was significantly greater with the oxygenated solution[in 10 recovered hearts] than the nonoxygenated solution[in 8 recovered hearts] [95.9$\pm$1.8% compared with 88.5$\pm$2.9% in peak aortic pressure, p<0.05, 75.7$\pm$5.2% compared with 43.5$\pm$6.5% in aortic flow, p<0.01, 75.5$\pm$4.6% compared with 54.1$\pm$5.6% in cardiac output, p<0.01, 78.3$\pm$4.6% compared with 60.3$\pm$4.6% compared with 60.3$\pm$6.2% in stroke volume, p<0.05, and 80.4$\pm$5.3% compared with 58.6$\pm$7.0% in dP/dT, p<0.05]. It is concluded that oxygenation of St. Thomas Hospital No.2 cardioplegic solution improves cardiac electrical stability and postischemic hemodynamic recovery after ischemic arrest in the isolated perfused rat heart.

• Journal of Chest Surgery
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• v.25 no.2
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• pp.131-136
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• 1992

The effect of temperature of cardioplegic solution on myocardial preservation was studied using isolated rat heart perfusion technique. Twenty Sprague-Dawley rats, weighing 120~140gm, were pretreated with intraperitoneal injection of heparin sodium[300u/kg] and then the hearts were excised after cervical herniation 30 minutes later. The hearts were perfused in isolated working heart apparatus with oxygenated modified Tyrode solution at 37oC. After 10 minutes of non working heart perfusion, the hearts were subjected to arrest for 30 minutes by administration of 5cc cardioplegic solution at the temperature of 4oC [Group I ], 15oC [Group II], 25oC [Group III], 37oC[Group IV]. At the same time, the topical cooling of heart was performed using ice saline. After arrest, the hearts were reperfused by non working heart perfusion for 1 hour with modified Tyrode solution at 37oC. The CPK, GOT and LDH in reperfusate were measured at 5,20,40,60 minutes after start of reperfusion. With the values of those, we compared the effect of temperature of cardioplegic solution on myocardial preservation. The results were as follows; 1. The enzyme values in reperfusate were highest at 5 minute and after then declined. 2. At 5 minutes after reperfusion, the enzyme values in Group I were lower than those in other Groups. These results suggest that the cardioplegic solutions using for cardiac arrest and myocardial protection can be working better at 4oC than at any other temperature.

• Korean Circulation Journal
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• v.48 no.12
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• pp.1081-1096
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• 2018

We reviewed the anatomical characteristics of the conduction system in the ventricles of human and ungulate hearts and then raised some questions to be answered by clinical and anatomical studies in the future. The ventricular conduction system is a 3-dimensional structure as compared to the 2-dimensional character of the atrial conduction system. The proximal part consisting of the atrioventricular node, the bundle of His and fascicles are groups of conducting cells surrounded by fibrous connective tissue so as to insulate from the underlying myocardium. Their location and morphological characters are well established. The bundle of His is a cord like structure but the left and right fascicles are broad at the proximal and branching at the distal part. The more distal part of fascicles and Purkinje system are linear networks of conducting cells at the immediate subendocardium but the intra-mural network is detected at the inner half of the ventricular wall. The papillary muscle also harbors Purkinje system not in the deeper part. It is hard to recognize histologically in human hearts but conducting cells as well as Purkinje cells are easily recognized in ungulate hearts. Further observation on human and ungulate hearts with myocardial infarct, we could find preserved Purkinje system at the subendocardium in contrast to the damaged system at the deeper myocardium. Further studies are necessary on the anatomical characteristics of this peripheral conduction system so as to correlate the clinical data on hearts with ventricular arrhythmias.

• Korean Journal of Veterinary Research
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• v.38 no.1
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• pp.29-42
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• 1998

$Mg^{2+}$ is one of the most abundant divalent cations in mammalian body(0.2~1.0mM) and the important physiological roles are : first, the cofactor of many enzyme activities, second, the regulator of glycolysis and DNA synthesis, third, the important role of bioenergetics by regulating of phosphorylation, fourth, the influence of cardiac metabolism and function. In this work we have investigated the regulation of the $Mg^{2+}$ induced by ${\alpha}_1-adrenoceptor$ stimulation in perfused guinea pig hearts and isolated myocytes. The $Mg^{2+}$ content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. The elimination of $Mg^{2+}$ in the medium increased the force of contraction of right ventricular papillary muscles, and the left ventricular pressure. Phenylephrine also enhanced the force of contraction in the presence of $Mg^{2+}-free$ medium. ${\alpha}_1-Agonists$ such as phenylephrine and methoxamine were found to induce $Mg^{2+}$ efflux in both perfused hearts and myocytes. These effects were blocked by prazosin, an ${\alpha}_1-adrenoceptor$ antagonist. The $Mg^{2+}$ influx could also be induced by phenylephrine and R59022, a diacylglycerol kinase inhibitor. In the presence of protein kinase C(PKC) inhibitors, phenylephrine produced an increase in $Mg^{2+}$ efflux from perfused hearts. Furthermore, $Mg^{2+}$ efflux by phenylephrine was amplified by phorbol 12-myristate 13-acetate(PMA). This enhancement of $Mg^{2+}$ efflux by PMA was blocked by prazosin in perfused hearts. By contrast, the $Mg^{2+}$ influx could be induced by verapamil, nifedipine, ryanodine in perfused hearts, but not in myocytes. $W^7$, a $Ca^{2+}$/calmodulin antagonist, completely blocked the phenylephrine-induced $Mg^{2+}$ efflux in perfused hearts. In conclusion, $Mg^{2+}$ is responsible for the cardiac activity associated with ${\alpha}_1-adrenoceptor$ stimulation. The mobilization of $Mg^{2+}$ is decreased or increased by ${\alpha}_1-adrenoceptor$ stimulation in guinea pig hearts. These responses may be related specifically to the respective pathways of signal transduction. A decrease in $Mg^{2+}$ efflux by ${\alpha}_1-adrenoceptor$ stimulation in hearts can be through PKC dependent and intracellular $Ca^{2+}$ levels.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.319-325
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• 2001

Several recent studies demonstrate that cAMP accumulation evokes marked changes in magnesium ($Mg^{2+}$) homeostasis. The goal of this study was to investigate the effect of melatonin, the principal hormone of the vertebral pineal gland, on $Mg^{2+}$ regulation in perfused guinea pig hearts. We hypothesized that melationin would regulate $Mg^{2+}$ efflux induced by adrenergic drugs and cAMP analogues because melatonin inhibites adneylate cyclase (AC) and phospholipase C(PLC) in the hearts. The $Mg^{2+}$ content in the perfusate was significantly higher in the presence than in the absence of melatonin. The addition of forskolin, isoproterenol or dimaprit to perfused hearts induced a marked $Mg^{2+}$ efflux. These effluxes were not inhibited by melatonin. The $Mg^{2+}$ efflux could also be induced by phenylephrine, a ${\alpha}_1$-adrenoceptor agonist. This phenylephrine-induced $Mg^{2+}$ efflux was inhibited by melatonin. In addition, the phenylephrine-induced $Mg^{2+}$ efflux was potentiated by PMA, a protein kinase C(PKC) activator. This $Mg^{2+}$ efflux was inhibited by melatonin. In conclusion, these data suggest that melatonin regulates $Mg^{2+}$ homeostasis and the inhibitory effect of melatonin on ${\alpha}_1$-adrenoceptor-stimulated $Mg^{2+}$ efflux may occur through an inhibition of PLC pathway in perfused guinea pig hearts.

• Journal of Chest Surgery
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• v.20 no.4
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• pp.643-654
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• 1987

The effect of prostacyclin[PGI, ] on myocardial preservation during global ischemia was studied in the isolating working rabbit heart model. Forty hearts underwent a 15 minute period of retrograde nonworking perfusion with Krebs-Henseleit buffer solution [37*C] and were switched over to the working mode for 15 minutes. After baseline measurement of heart rate, peak aortic pressure, aortic flow, and coronary flow, all hearts were subjected to 60 minutes of ischemic arrest at 10*C induced with St. Thomas Hospital cardioplegic solution: Group I had single dose cardioplegia, Croup II double dose, Croup III oxygenated double dose, and Group IV single dose with PCI, infusion [10ng/min./gm heart weight]. Hearts were then revived with 15 minute period of nonworking reperfusion at normothermia, followed by 30 minutes of working perfusion. Repeat measurements of cardiac function were obtained and expressed as a percent of the preischemic baseline values. Oxygen content of arterial perfusate and coronary effluent was measured by designed time interval. Leakage of creatine kinase was determined during post-ischemic reperfusion period. Finally wet hearts were weighed and placed in 120*C oven for 36 hours for measurement of dry weight. In the PGI, treated group [IV], heart rate increased consistently throughout the period of reperfusion from 100*5.0% [p<0.001] to 107*6.2% [p<0.001]. The percent recovery of aortic flow showed 95*5.7% [p<0.001] at the first 3 minute and full recovery through the subsequent time. Coronary flow was augmented significantly in the 3 minute [96*6.2%, p<0.001] and then sustained above baseline values. Among the Croup I, II, and III, all hemodynamic values were significantly below preischemic levels. PGI2 relatively increased oxygen delivery [1.22*0.19ml/min, p<0.001] and myocardial oxygen consumption [0.90*0.13ml/min, p<0.001] during reperfusion period. Leakage of creatine kinase in the PGI2 group was 9.3*1.58IU/15min [p<0.001]. This was significantly lower than Group I [33.0*2.68 IU/15min]. The water content of PCI2 treated hearts [81*0.9%, p<0.001] was also lower than the other groups.

• Applied Microscopy
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• v.20 no.1
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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.

• Journal of Pharmacopuncture
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• v.21 no.3
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• pp.159-167
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• 2018

Objectives: Myocardial reperfusion is the only logical cure for ischemic heart disease. However, ischemic-reperfusion (I/R) injury is one of the underlying factors facilitating and accelerating the apoptosis in the myocardium. This study set to investigate the impact of Teucrium polium (TP) hydro-alcoholic extract on I/R induced apoptosis in the isolated rat heart. Methods: Isolated rat hearts were classified into six groups. The control samples were subjected to 80 min of perfusion with Krebs-Henseleit bicarbonate (KHB) buffer; in control-ischemia group, after primary perfusion (20 min) the hearts were exposed to global ischemia (20 min) and reperfusion (40 min). Pretreated groups were perfused with $500{\mu}M$ of vitamin C and various TP concentrations (0.5, 1, 2 mg/ml) for 20 min, and then the hearts were exposed to ischemia and reperfusion for 20 min and 40 min, respectively. Cardiodynamic parameters including rate pressure product (RPP), heart rate (HR), the maximum up/down rate of left ventricular pressure (${\pm}dp/dt$), left ventricular developed pressure (LVDP), and coronary artery flow (CF) were achieved from Lab Chart software data. The Bax and BCl-2 gene expressions were measured in heart samples. Results: Hearts treated with TP extract and vit C represented a meaningful improvement in cardiac contractile function and CF. The overexpression of Bcl-2, downregulation of Bax, and improvement of apoptotic index (Bax/Bcl-2) were observed in pretreated TP extract and vit C hearts. Conclusion: The TP extract was found to ameliorate the cardiac function in the reperfused myocardium. Also, it can hinder apoptotic pathways causing cardioprotection.

• Journal of applied mathematics & informatics
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• v.30 no.3_4
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• pp.413-428
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• 2012

Every contingent claim is unable to be replicated in the incomplete markets. Shortfall risk is considered with some risk exposure. We show how the dynamic optimization problem with the capital constraint can be reduced to the problem to find an optimal modified claim $\tilde{\psi}H$ where$\tilde{\psi}H$ is a randomized test in the static problem. Convex and coherent risk measures defined in the Orlicz hearts spaces, $M^{\Phi}$, are used as risk measure. It can be shown that we have the same results as in [21, 22] even though convex and coherent risk measures defined in the Orlicz hearts spaces, $M^{\Phi}$, are used. In this paper, we use Fenchel duality Theorem in the literature to deduce necessary and sufficient optimality conditions for the static optimization problem using convex duality methods.