• Journal of Chest Surgery
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• v.31 no.2
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• pp.95-101
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• 1998

Ischemic preconditioning is known to have protective effect on myocardial function at prolonged ischemic insult but the mechanism of the effect is not clearly known. The effect of the preconditioning on the global ischemia using cardioplegic solution is not well known. To evaluate the effect of global myocardial preconditioning on the functional recovery after cardioplegic arrest and two hours of hypothermic storage, we used the isolated rat heart and two hours cardioplegic arrest time at $0^{\circ}C$. In the experimental group(n=10), after baseline functional data was obtained, ischemic preconditioning was induced with 1 min of global normothermic ischemia for three times before the arrest period. In the control group(n=10), hearts underwent no ischemic precondi- tioning. After 2 hrs of cardioplegic arrest and storage in the $0^{\circ}C$ cardioplegic solution reperfusion was done and hemodynamic data were collected at post-reperfusion 20 min. Heart with ischemic preconditioning showed improved functional recovery at post reperfusion 20 min in peak developed pressure and dP/dT. In percent change of the peak pressure, preconditioning group showed 93.20$\pm$15.7% recovery rate compared to baseline data, and control group showed 67.3$\pm$15.6% recovery rate. In percent change of the dP/dT, control group showed 54.7$\pm$18.2% recovery rate and preconditioning group showed 78.1$\pm$15.1% recovery rate. Percent changes in heart rate and coronary flow showed no significant difference between two groups and there was no significant differences in amount of cardioplegic delivery between groups. Our data suggest ischemic preconditioning may have protective effect on recovery state after cardioplegic arrest and 2 hr ischemic storage of isolated rat heart and its mechanism is not related to the amount of the cardioplegic delivery amount.

• Journal of the Korean Society of Radiology
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• v.81 no.2
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• pp.250-271
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• 2020

Assessment of myocardial ischemia in patients with stable angina is important in deciding whether to treat coronary artery disease and in predicting clinical outcome. The fractional flow reserve is a standard reference for the diagnosis of myocardial ischemia, but this procedure has limitations because of its invasiveness. Coronary computed tomography angiography (CCTA) is now an established tool in the anatomic diagnosis of coronary artery disease; however, there are limits to the diagnosis of hemodynamically important stenosis that causes myocardial ischemia. In order to address this problem, studies using quantification of coronary atherosclerotic plaques, myocardial perfusion, and noninvasive calculation of fractional flow reserve based on CCTA have been actively conducted and recognized for their diagnostic value. In this review, several imaging techniques of CCTA used to assess myocardial ischemia are described.

• Journal of Chest Surgery
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• v.31 no.10
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• pp.924-927
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• 1998

Background: Myocardial cell death after myocardial infarction or reperfusion is classified into necrosis and apoptosis. Bcl-2 protein is a cytoplasmic protein, which inhibits apoptosis and is expressed in acute stage of myocardial infarction but not in normal heart. This study was performed to investigate whether Bcl-2 protein was expressed respectively to the reperfusion time. Materials and methods: Thirty nine New Zealand white rabbits weighing 1.5-4.8 kg (mean, 2.9kg) were alloted into 7 groups (n=5 in each group) which underwent left anterior descending coronary artery(LAD) occlusion for 30 minutes, followed by reperfusion. The animals were sacrificed at 1, 4, 8, 12, 24 hours, and 3, 7 days after occlusion. Ventricle was excised immediately after intervention. Tissues were fixed in 10% buffured formalin and embedded in paraffin. Bcl-2 protein was detected by immunohistochemical stain with using monoclonal antibody against Bcl-2 protein. Results: The positive immunohistochemical reactivity for Bcl-2 protein was observed in 12, 24 hours, and 3 days reperfusion groups. Bcl-2 protein was detected in salvaged myocytes surrounding the infarcted area. Conclusions: Bcl-2 protein is expressed at the late acute stage of infarct. Therefore, the expression of Bcl-2 protein may not protect acute cell death, but may play a role in the prevention of late cell death after myocardial is chemia-reperfusion.

• Journal of Chest Surgery
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• v.31 no.8
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• pp.739-748
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• 1998

Background: It has been well documented that transient occlusion of the coronary artery causes myocardial ischemia and finally cell death when ischemia is sustained for more than 20 minutes. Extensive studies have revealed that ischemic myocardium cannot recover without reperfusion by adequate restoration of blood flow, however, reperfusion can cause long-lasting cardiac dysfunction and aggravation of structural damage. The author therefore attempted to examine the effect of postischemic reperfusion on myocardial ultrastructure and to determine the rationales for recanalization therapy to salvage ischemic myocardium. Materials and methods: Young Holstein-Friesian cows(130∼140 Kg body weight; n=40) of both sexes, maintained with nutritionally balanced diet and under constant conditions, were used. The left anterior descending coronary artery(LAD) was occluded by ligation with 4-0 silk snare for 20 minutes and recanalized by release of the ligation under continuous intravenous drip anesthesia with sodium pentobarbital(0.15 mg/Kg/min). Drill biopsies of the risk area (antero-lateral wall) were performed at just on reperfusion(5 minutes), 1-, 2-, 3-, 6-, 12-hours after recanalization, and at 1-hour assist(only with mechanical respiration and fluid replacement) after 12-hour recanalization. The materials were subdivided into subepicardial and subendocardial tissues. Tissue samples were examined with a transmission electron microscope (Philips EM 300) at the accelerating voltage of 60 KeV. Results: After a 20-minute ligation of the LAD, myocytes showed slight to moderate degree of ultrastructural changes including subsarcolemmal bleb formation, loss of nuclear matrix, clumping of chromatin and margination, mitochondrial destruction, and contracture of sarcomeres. However, microvascular structures were relatively well preserved. After 1-hour reperfusion, nuclear and mitochondrial matrices reappeared and intravascular plugging by polymorphonuclear leukocytes or platelets was observed. However, nucleoli and intramitochondrial granules reappeared within 3 hours of reperfusion and a large number of myocytes were recovered progressively within 6 hours of reperfusion. Recovery was apparent in the subepicardial myocytes and there were no distinct changes in the ultrastructure except narrowed lumen of the microvessels in the later period of reperfusion. Conclusions: It is likely that the ischemic myocardium could not be salvaged without adequate restoration of coronary flow and that the microvasculature is more resistant to reversible period of ischemia than subendocardium and subepicardium. Therefore, thrombolysis and/or angioplasty may be a rational method of therapy for coronarogenic myocardial ischemia. However, it may take a relatively longer period of time to recover from ischemic insult and reperfusion injury should be considered.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.321-330
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• 1994

The protective effect of 'ischemic preconditioning (PC)' on ischemia-reperfusion injury of heart has been reported in various animal species, but without known mechanisms in detail. In an attempt to investigate the cardioprotective mechanism of PC, we examined the effects of PC on the myocardial oxidative injuries and the oxygen free radical production in the ischemia-reperfusion model of isolated Langendorff preparations of rat hearts. PC was performed with three episodes of 5 min ischemia and 5 min reperfusion before the induction of prolonged ischemia (30 min)-reperfusion(20 min). PC prevented the depression of cardiac function (left ventricular pressure x heart rate) observed in the ischemic-reperfused heart, and reduced the release of lactate dehydrogenase during the reperfusion period. On electron microscopic pictures, myocardial ultrastructures were relatively well preserved in PC hearts as compared with non-PC ischemic-reperfused hearts. In PC hearts, lipid peroxidation of myocardial tissue as estimated from malondialdehyde production was markedly reduced. PC did not affect the activity of xanthine oxidase which is a major source of oxygen radicals in the ischemic rat hearts, but the myocardial content of hypoxanthine (a substrate for xanthine oxidase) was much lower in PC hearts. It is suggested from these results that PC brings about significant myocardial protection in ischemic-reperfused heart and this effect may be related to the suppression of oxygen free radical reactions.

• Journal of Chest Surgery
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• v.39 no.7 s.264
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• pp.549-552
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• 2006

In the mitral regurgitation (MR) accompanied with a serious ischemic cardiomyopathy (ICMP), coronary revascularization to viable myocardium, LV reduction and mitral reconstruction become the main surgery under the bad conditions that the cardiac transplantation is not so easy. The MR in ischemic cardiomyopathy appears as various pathologic factors, among them, the papillary muscle displacement in addition to the annular dilatation is pointed out as the important cause. Our hospital would like to report the experience of the surgery about coronary revascularization to the left main with 3-vessel coronary disease, severe ICMP patients accompanied with the MR, posterior mitral annuloplasty and papillary muscle plication through the LVtomy.

• 순환기질환의공학회:학술대회논문집
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• 2005.05a
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• pp.79-88
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• 2005

• Journal of Chest Surgery
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• v.29 no.8
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• pp.807-815
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• 1996

The protective effect of'ischemic preconditioning'on ischemid-reperfusion injury of heart has been reported in various animal species. but without known mechAnism in detail, In An attempt to investigate the cardioprotective mechanism of ischemic preconditioning, we examined the effects of nitric oxide(UO) synthesis in preconditioned heart of rat The isolated hearts perfused by Langendorfr's method were ex- posed to 30min global ischemia followed by 30min reperfusion with oxygenated Krebs-Henseleit(K-H) sol- ution. Ischemic preconditioning was performed with three episodes of Sm n ischemia and Smin repeyfusion before the induction of prolong ischemia(30min)-reperfusion(30min). Ischemic preconditioning prevented the depression of cardiac function(left ventricular pressure .K heart rate) observed in the ischemia- reperfusion hearts and reduced the release of lactate dehydrogenase during the reperfusion period. On electromicroscopic pictures, myocardial ultrastructures wore relatively well preserved in isthemic preconditioned hearts. N6_nitro-L-arginine methyl ester(L-NAME) an inhibitor of L-arginine citric oxide pathway, was infused at a rate O.Smllmin In a dose of 10mg kg-1 before the initial ischemic preconditioning. neither the protection of cardiac function nor the reduction of LDH releAse in ischemic preconditioning hearts was altered in the presence of added L-NAME On ultrastructural finding, the preservation of morphology in ischemic preconditioning heart was not change by the pretreatment of L-UAME. The failure of the WO synthesis inhibitor to reduce t e effect of ischemic preconditioning may be related to be species specific in that NO may allot be the trigger for ischemic preconditioning in rats.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.603-612
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• 1999

Background : It has been documented that brief repetitive periods of ischemia and reperfusion (ischemic preconditioning, IP) enhances the recovery of post-ischemic contractile function and reduces infarct size after a longer period of ischemia. Many mechanisms have been proposed to explain this process. Recent studies have suggested that transient increase in the intracellular calcium may have triggered the activation of protein kinase C(PKC); however, there are still many controversies. Accordingly, the author performed the present study to test the hypothesis that preconditioning with high concentration of calcium before sustained subsequent ischemia(calcium preconditioning) mimics IP by PKC activation. Material and Method : The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) Method: The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to 45-minute global ischemia followed by a 120-minute reperfusion with IP(IP group, n=13) or without IP(ischemic control, n=10). IP was induced by single episode of 5-minute global ischemia and 10-minute reperfusion. In the Ca2+ preconditioned group, perfusate containing 10(n=10) or 20 mM(n=11) CaCl2 was perfused for 10 minutes after 5-minute ischemia followed by a 45-minute global ischemia and a 120-minute reperfusion. Baseline PKC was measured after 50-minute perfusion without any treatment(n=5). Left ventricular function including developed pressure(LVDP), dP/dt, heart rate, left ventricular end-diastolic pressure(LVEDP) and coronary flow(CF) was measured. Myo car ial cytosolic and membrane PKC activities were measured by 32P-${\gamma}$-ATP incorporation into PKC-specific pepetide. The infarct size was determined using the TTC (tetrazolium salt) staining and planimetry. Data were analyzed using one-way analysis of variance(ANOVA) variance(ANOVA) and Tukey's post-hoc test. Result: IP increased the functional recovery including LVDP, dP/dt and CF(p<0.05) and lowered the ascending range of LVEDP(p<0.05); it also reduced the infarct size from 38% to 20%(p<0.05). In both of the Ca2+ preconditioned group, functional recovery was not significantly different in comparison with the ischemic control, however, the infarct size was reduced to 19∼23%(p<0.05). In comparison with the baseline(7.31 0.31 nmol/g tissue), the activities of the cytosolic PKC tended to decrease in both the IP and Ca2+ preconditioned groups, particularly in the 10 mM Ca2+ preconditioned group(4.19 0.39 nmol/g tissue, p<0.01); the activity of membrane PKC was significantly increased in both IP and 10 mM Ca2+ preconditioned group (p<0.05; 1.84 0.21, 4.00 0.14, and 4.02 0.70 nmol/g tissue in the baseline, IP, and 10 mM Ca2+ preconditioned group, respectively). However, the activity of both PKC fractions were not significantly different between the baseline and the ischemic control. Conclusion: These results indicate that in isolated Langendorff-perfused rabbit heart model, calcium preconditioning with high concentration of calcium does not improve post-ischemic functional recovery. However, it does have an effect of limiting(reducing) the infart size by ischemic preconditioning, and this cardioprotective effect, at least in part, may have resulted from the activation of PKC by calcium which acts as a messenger(or trigger) to activate membrane PKC.

• 대한핵의학회:학술대회논문집
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• 2002.11a
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• pp.34.2-34.2
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• 2002