• Title/Summary/Keyword: Myocardial reperfusion

검색결과 155건 처리시간 0.033초

허혈심근 Xanthine Oxidase 의 전환에 관한 연구 (Conversion of Myocardial Xanthine Oxidase in Ischemic Heart of Rat)

  • 박창권
    • Journal of Chest Surgery
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    • 제21권5호
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    • pp.803-815
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    • 1988
  • The present experiments were performed to confirm the hypothesis that xanthine oxidase[XOD], as a source and mechanism of oxygen radical production, plays an important role in the genesis of the reperfusion injury of ischemic myocardium. The experimental ischemic-reperfusion injury was induced in isolated, Langendorff preparations of rat hearts by 60 min. Of global ischemia with aortic clamping followed by 20 min. of reperfusion with oxygenated Krebs-Henseleit solution[pH 7.4, 37*C]. The results were as follows: 1. The releases of creatine phosphokinase and a lipid peroxidation product, malondialdehyde[MDA] into the coronary effluent were abruptly increased upon reperfusion of ischemic hearts. The increases of the enzyme and MDA were suppressed significantly in the hearts removed from rats pretreated with allopurinol, a specific XOD inhibitor[20mg/kg, oral, 24 hrs and 2 hrs before study]. This effect of allopurinol was comparable to that of oxygen radical scavengers, superoxide dismutase[5, 000U] and catalase[12, 500 U]. 2. The increased SOD-inhibitable reduction of ferricytochrome C, which was infused to the hearts starting with reperfusion, was significantly suppressed in allopurinol pretreated hearts. 3. Activities of myocardial XOD were compared in the normal control hearts and the ischemic ones. Total enzyme activities were not different in both hearts. However, comparing with the control, the ischemic ones showed higher activity in 0-form and lower activities in D-form and D/O-form. 4. In the ischemic hearts, phenylmethylsulfonyl fluoride, a serine protease inhibitor, prevented significantly the increase of 0-form and the decreases of D and D/O-form, while thiol reagents did not affect the changes of the enzyme. 5. The increase of 0-form and the decreases of D and D/0-form were not significant in both calcium-free perfused and pimozide, a calmodulin inhibitor, treated ischemic hearts. 6. The SOD-inhibitable reduction of ferricytochrome C were suppressed by PMSF and pimozide treatment as well as by calcium-free perfusion. It is suggested from these results that in the ischemic rat myocardium, xanthine oxidase is converted to oxygen radical producing 0-form by calcium, calmodulin-dependent proteolysis and plays a contributing role in the genesis of ischemic-reperfusion injury by producing oxygen free radicals.

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Teucrium polium L. Improved Heart Function and Inhibited Myocardial Apoptosis in Isolated Rat Heart Following Ischemia-Reperfusion Injury

  • Mahmoudabady, Maryam;Talebian, Faezeh Sadat;Zabihi, Narges Amel;Rezaee, Seyed Abdolrahim;Niazmand, Saeed
    • 대한약침학회지
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    • 제21권3호
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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.

Apple pectin, a dietary fiber, ameliorates myocardial injury by inhibiting apoptosis in a rat model of ischemia/reperfusion

  • Lim, Sun Ha;Kim, Mi Young;Lee, Jongwon
    • Nutrition Research and Practice
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    • 제8권4호
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    • pp.391-397
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    • 2014
  • BACKGROUND/OBJECTIVE: Myocardial cell death due to occlusion of the coronary arteries leads to myocardial infarction, a subset of coronary heart disease (CHD). Dietary fiber is known to be associated with a reduced risk of CHD, the underlying mechanisms of which were suggested to delay the onset of occlusion by ameliorating risk factors. In this study, we tested a hypothesis that a beneficial role of dietary fiber could arise from protection of myocardial cells against ischemic injury, manifested after occlusion of the arteries. MATERIALS/METHODS: Three days after rats were fed apple pectin (AP) (with 10, 40, 100, and 400 mg/kg/day), myocardial ischemic injury was induced by 30 min-ligation of the left anterior descending coronary artery, followed by 3 hr-reperfusion. The area at risk and infarct area were evaluated using Evans blue dye and 2,3,5-triphenyltetrazolium chloride (TTC) staining, respectively. DNA nicks reflecting the extent of myocardial apoptosis were assessed by TUNEL assay. Levels of cleaved caspase-3, Bcl-2, and Bax were assessed by immunohistochemistry. RESULTS: Supplementation of AP (with 100 and 400 mg/kg/day) resulted in significantly attenuated infarct size (IS) (ratio of infarct area to area at risk) by 21.9 and 22.4%, respectively, in the AP-treated group, compared with that in the control group. This attenuation in IS showed correlation with improvement in biomarkers involved in the apoptotic cascades: reduction of apoptotic cells, inhibition of conversion of procaspase-3 to caspase-3, and increase of Bcl-2/Bax ratio, a determinant of cell fate. CONCLUSIONS: The findings indicate that supplementation of AP results in amelioration of myocardial infarction by inhibition of apoptosis. Thus, the current study suggests that intake of dietary fiber reduces the risk of CHD, not only by blocking steps leading to occlusion, but also by protecting against ischemic injury caused by occlusion of the arteries.

In-111-Antimyosin 항체를 이용한 심근경색의 정량적 평가 (Quantitative Assessment of Myocardial Infarction by In-111 Antimyosin Antibody)

  • 이명철;이경한;최윤호;정준기;박영배;고창순;문대혁
    • 대한핵의학회지
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    • 제25권1호
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    • pp.37-45
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    • 1991
  • Infarct size is a major determinant of prognosis after acute myocardial infarction. Up to date, however, clinically available tests to estimate this size have not been sufficiently accurate. Twelve lead electrocardiogram and wall motion abnormality measurement are not quantitative, and creatine phophokinase (CPK) measurement is inaccurate in the presence of reperfusion or right ventricular infarction. Methods have been developed to localize and size acute myocardial infarcts with agents that are selectively sequestered in areas of myocardial damage, but previously used agents have lacked sufficient specificity. Antibodies that bind specifically only to damaged myocardial cells may resolve this problem and provide an accurate method for noninvasively measuring infarct size. We determined the accuracy with which infarcted myocardial mass can be measured using single photon emission computed tomography (SPECT) and radiolabeled antimyosin antibodies. Seven patients with acute myocardial infarction and one stable angina patient were injected with 2 mCi of Indium-111 labeled antimyosin antibodies. Planar image and SPECT was performed 24 hours later. None of the patients had history of prior infarcts, and none had undergone reperfusion techniques prior to the study, which was done within 4 days of the attack. Planar image showed all infarct patients to have postive uptakes in the cardiac region. The location of this uptake correlated to the infarct site as indicated by electrocardiography in most of the cases. The angina patient, however, showed no such abnormal uptake. Infarct size was determined from transverse slices of the SPECT image using a 45% threshold value obtained from a phantom study. Measured infarct size ranged from 40 to 192 gr. There was significant correlation between the infarct size measured by SPECT and that estimated from serial measurements of CPK (r=0.73, p<0.05). These date suggest that acute myocardial infarct size can be accurately measured from SPECT Indium-111 antimyosin imaging. This method may be especially valuable in situations where other methods are unreliable, such as early reperfusion technique, right ventricular infarct or presence of prior infarcts.

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Effect of Ursodeoxycholic Acid on Ischemia/Reperfusion Injury in Isolated Rat Heart

  • Lee, Woo-Yong;Han, Suk-Hee;Cho, Tai-Soon;Yoo, Young-Hyo;Lee, Sun-Mee
    • Archives of Pharmacal Research
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    • 제22권5호
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    • pp.479-484
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    • 1999
  • In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

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재관류시 외인성 칼슘 자극이 허혈 심근에 미치는 영향에 대한 전자현미경적 연구 (An Ultrastructural Study on the Effect of Exogenous $Ca^{2+}$ Stimulation to Ischemic Myocardium during Post-ischemic Reperfusion)

  • 김호덕;전상배;라봉진
    • Applied Microscopy
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    • 제21권1호
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    • pp.1-20
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    • 1991
  • The effects of exogenous $Ca^{2+}$ stimulation on the post-ischemic myocardial cells were studied using isolated Langendorff-perfused guinea pig hearts. At the starting point of reperfusion, Tyrode solutions, each containing 2.0mM, 4.0mM and 8.0mM $CaCl_2$ respectively, were administered for 2 minutes apart by descending, ascending, or by combined sequences followed by standard Tyrode solution containing 1.0mM $CaCl_2$. The minutes of global ischemia produced reversible but moderate to severe degree of myocardial ultrastructrual changes including focal destruction of sarcolemma, loss of nuclear matrix, clumping and margination of chromatins, mitochondrial swelling, destruction of mitochondrial cristae, shortening of sarcomeres, focal loss of myofibrils, and separation of cell junctions. In spite of reperfusion, the ultrastructure was more severely damaged and irreversible changes such as intracellular fluid accumulation, contracted sarcomeres, mitochondrial destruction, disruption of sarcolemma, loss of nuclear matrix, and separation of cell junction were observed in a large number of cells. In contrast, Tyrode-perfused $Ca^{2+}$-stimulated myocardial cells showed relatively well preserved ultrastucture, except slight changes including focal mitochondrial swelling, widening of T-tubule, and widening of cell junctions, especially at fasciae adherentes. The post-ischemic $Ca^{2+}$-stimulated reperfused myocardial cells produced focal changes such as mitochondrial destruction, disintegration of sarcolemma, widening of T-tubule, and intracellular fluid accumulation with slight variation in degree of changes by the method of $Ca^{2+}$ administration sequence. However, in a large number of the myocardial cells, chromatins were redistributed relatively evenly in the nuclear matrix, mitochondrial cristae were tightly packed, and a considerable number of intramitochondrial granules and glycogen granules reap-pealed. These results indicate that exogenous $Ca^{2+}$ stimulation in the initial period of reperfusion may be beneficial to salvage or to reduce the post-ischemic myocardium from further deleterious changes, and that the beneficial effects may be derived from the reserves of the function of the intracellular $Ca^{2+}$ regulating organelles and/or from the responsiveness of contractile apparatus to $Ca^{2+}$ stimulation.

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심정지액 속에 포함된 아데노신의 용량에 따른 심근보호 효과 비교 (The Comparison of Protective Effects of Adenosine Included Cardioplegia According to Adenosine Dosage)

  • 유경종;강면식;이교준;임상현;박한기;김종훈;조범구
    • Journal of Chest Surgery
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    • 제31권9호
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    • pp.837-844
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    • 1998
  • 배경: 아데노신은 심근의 허혈상태에서 심근세포로부터 분비되어 부정맥과 심근허혈 및 수술후 재관류손상을 억제시키는 호르몬으로 알려져 있다. 아데노신의 심근보호 효과에 대한 연구는 주로 심정지액 속에 포함시킨 아데노신의 효과에 대하여 이루어 지고 있으나, 심정지액 속에 포함된 아데노신의 적정용량에 대해서는 보고가 다양하다. 저자들은 자체제작한 심폐체외순환 모델을 이용하여 단일용량의 아데노신(0.75 mg/Kg/min)이 우수한 심근보호효과를 나타낸 결과를 보고한 바 있으나 적절한 용량이었는지에 대한 확신은 없다. 따라서 본 연구의 목적은 심정지액 속에 포함된 아데노신의 적정용량을 알아보는데 있다. 대상 및 방법: 연구방법은 쥐를 이용하여 심정지시 심정지액(St. Thomas 심정지액)에 첨가한 아데노신의 용량에 따라 1군(0.5 mg/Kg/min), 2군(0.75 mg/Kg/min) 및 3군(1 mg/Kg/min) 으로 나누어 각각 10마리씩 실험하여 비교하였다. 마취 후 적출된 쥐심장의 대동맥과 좌심방에 도관을 삽관한 후에 심폐체외순환 모델에 연결하여 비작업성 순환과 작업성 순환을 시행하면서 혈역학적 수치를 측정하여 이를 대조값으로 이용하였다. 심정지액을 주입하여 심정지를 유도한 후에 90분간 허혈상태로 유지한 다음 비작업성 순환을 시행 후 작업성 순환으로 바꿔 10분, 30분 및 60분에 혈역학적 수치(심박동수, 수축기 대동맥압, 1분간 대동맥 박출량 및 관동맥관류량)를 측정하고, 생화학적 검사(CPK, Lactic Acid) 및 심장의 수분함유량도 측정하였다. 측정된 수치는 심정지 전 측정한 대조값에 대한 백분율로 환산하여 비교하였다. 결과: 실험 결과 심정지 전에 측정한 대조값 사이에는 세군 사이의 통계적인 유의성이 없었다. 심정지액의 주입 후 3군에서 가장 빨리 심정지가 일어났으며(p<0.05), 재관류 후 심박동이 돌아온 시간은 1군과 2군이 3군에 비하여 통계학적으로 유의하게 심박동이 빨리 돌아 왔다 (p<0.05). 그러나 1군과 2군 사이에는 유의성이 없었다. 심장의 재관류 후 측정한 심박동수의 회복률에서 10분에 측정한 값은 세군 사이에 유의성이 없었으나, 30분과 60분 에 측정한 값은 1군이 2군과 3군에 비하여 유의하게 높았으며(p<0.05), 2군도 3군에 비하여 유의하게 높았다(p<0.05). 수축기 대동맥압의 회복률, 1분 동안의 대동맥 박출량 및 심박출량(1분 동안의 대동맥 박출량과 관동맥관류량을 합산한 값)은 10분, 30분 및 60분에서 모두 2군이 1군과 3군에 비하여, 1군은 3군에 비하여 유의하게 높았다(p<0.05). 관동맥관류량의 회복률은 10분과 30분에 측정한 값은 2군이 1군과 3군에 비하여, 1군은 3군에 비하여 유의하게 높았으며(p<0.05), 60분에 측정한 값은 1군과 2군이 3군에 비하여 유의하게 높았다(p<0.05). 심근의 수분함유량과 관상동맥 관류량의 생화학적 검사결과 CPK와 Lactic Acid는 세군 사이에 유의성이 없었다. 결론 : 이상의 결과로 아데노신을 심정지용액에 첨가시 비교적 적정 용량은 0.75 mg/Kg/min 을 투여하는 것이 적절할 것으로 생각된다.

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허혈전후 적출 가토 심근내의 구성 효소의 변화 (Pre-and Post-ishemic Changes of the Constituent Enzymes in Isolated Rabbit's Myocardium)

  • 천수봉;전도환;이재성;김송명
    • Journal of Chest Surgery
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    • 제33권2호
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    • pp.117-124
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    • 2000
  • Background: Nucleoside transport inhibitor(NTI) Keeps AMP, ADP, ATP levels high in myocytes by inhibiting adenosine cataboilsm so that it may preserve the myocardial contractability during ischemia In this study we investigated the effects of cyclic AMP phosphodiesterase inhibor(C-AMP PDSI) and S-P-nitrobenzyl-6 -thioniosine(NBT; a sort of NIT) on myocadial preservation and changes of constituent enzyme. Material and method: Twenty-six isolated rabbit hearts were perfused with Krebs-Henseleit buffer solution for 20 minutes arrested for 20 minutes and ten reperfused for 30 minutes. The following four groups were prepared and hemodynamic changes coronary effluent lactate dehydrogenase (LDH) a-hydroxybutylic accid(a-HBD) levels and myocardial LDH creatine kinase-MB (CK-MB) adenosine deaminase(ADA) a-HBD levels and myocardial LDH creatine kinase-MB (CK-MB) adenosine deaminase(ADA) a-HBD levels were analysed before and after cardiac arest ; Group I(control) ; the heart was only perfused with K-H ; Group II ; the heart was perfused with K-H including C-AMP PDSI(Amrinone 25mg/L); Group III ; the heart was perfused with K-H including NBT(4.19mg/L) ; Group IV ; the heart was perfused with K-H including C-AMP PDSI + NBT. Result : Left venticular developed pressure(LVDP) at 10 minutes of the equilibrium was significantly higher in group III(72.1$\pm$5.3 mmHg p<0.01) and group III(72$\pm$5.6 mmHg P<0.025) as compared with group I (40.8$\pm$4.7mmHg) and LVDP at 20 minutes of the reperfusion was significantly higher in group II(74$\pm$5.3mmHg p<0.01) and group III(72$\pm$5.6mmHg p<0.025) as compared with group I (44.2$\pm$4.6mmHg). Percentage recovery of LVDP at the reperfusion was the highest in group II(123.3%) Percentage recovery of coronary flow at the equilibrium reperfusion were higher in group II(310%, 270%) group III(230%, 290%) group IV(310%, 280%) as compared with group I (100%) respectively. Myocadial LDH level was significant lower in group IV(33495$\pm$1802 IU/gm p<0.04) as compared with group I(48767$\pm$1421 IU/gm) Myocadial CK-MB level was significant higher in group II(74820$\pm$1421 IU/gm) compared with group I (45450$\pm$1737 IU/gm) Myocadial ADA level was significant higher group IV(1215$\pm$8 IU/gm p<0.05) compared with group I(125$\pm$15 IU/gm) but there was no significant difference between group I and group II ,III, IV in changes of coronary effluent LDH, a-HBD levels. Conclusion: C-AMP PDSI solely appears to have a better effect on myocardial preservation after ischemia than NBT but with no synergistic effect and it could keep CK-MB leve high in myocardial tissues.

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흰쥐심장의 허혈손상에 대한 Calcium 통로봉쇄제와 Calmodulin 억제제의 예방효과에 대한 연구 (Prevention of Ischemic Damage in Working Rat Hearts by Calcium Channel Blocker and Calmodulin Inhibitors)

  • 성시찬
    • Journal of Chest Surgery
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    • 제22권6호
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    • pp.901-913
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    • 1989
  • This study was investigated under the postulation that activation of intracellular calcium- calmodulin complex during ischemia-reperfusion leads to myocardial injury. The protective effects of calcium channel blocker, diltiazem and calmodulin inhibitors, trifluoperazine, flunarizine and calmidazolium from ischemic injury in rat hearts were observed by using Langendorff apparatus when the antagonists were infused for 3 min in the beginning of ischemia. Thereby, an increase in resting tension developed during 30-min ischemia was analyzed with regard to [1] the degree of cardiac functional recovery following 60-min reperfusion, [2] changes in biochemical variables evoked during 30-min ischemia. The results obtained were as follows: l. In the ischemic group, the resting tension was increased by 4.1*0.2 g at 30-min ischemia. However, the increase in resting tension was markedly reduced not only by pretreatment with diltiazem [3.3 p M] but also with calmodulin inhibitors, trifluoperazine [3.3 p M], flunarizine [0.5 p M] and calmidazolium [0.5 p M], respectively. 2. Recovery of myocardial contractility, +dF /dt and coronary flow were much reduced when evoked by reperfusion in the ischemic group. These variables were significantly improved either by pretreatment with diltiazem or with calmodulin inhibitors. 3. The resting tension increment evoked during ischemia was significantly inversely correlated with the degree of cardiac function recovered during reperfusion. 4. Following 30-min ischemia, the production of malondialdehyde and release of lysosomal enzyme were much increased in association with a decrease in creatine kinase activity. 5. The increases in malondialdehyde production and release of free lysosomal enzyme were suppressed by pretreatment with calmodulin inhibitors as well as diltiazem. Likewise, the decrease of creatine kinase activities was prevented by these calcium antagonists. With these results, it is indicated that a increase in resting tension observed during ischemia has an inverse relationship to the cardiac function recovered following reperfusion, and further, the later may be significantly dependent on the degree of biochemical alterations occurred during ischemia such as decrease in creatine kinase activity, increased production of malondialdehyde and increased release of free lysosomal enzyme. Thus it is concluded that calmodulin plays a pivotal role in the process of ischemic injury.

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항산화제 Amifostine의 허혈 및 재관류시 흰쥐 적출심장의 심근 보호기능 (Cardioprotective Potency of the Antioxidante Amifostine in the Ischemic and Reperfused Isolated Rat Heart)

  • 허강배;천수봉;김송명
    • Journal of Chest Surgery
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    • 제31권9호
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    • pp.845-854
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    • 1998
  • Background: S-2-(3 aminoprophlamino) ethylphosphorothioic acid(WR-2721) is one of the radical scavenging thiols. We tested its protective effects in the reperfused heart. Material and Method: The experimental setup was the constant pressure Langendorffs perfusion system. We investigated the radical scavenging properties of this compound in isolated rat hearts which were exposed to 20 minutes ischemia and 20 minutes reperfusion. Four experimental groups were used:group I, control, Amifostine 50 mg(1 mL) peritoneal injection 30 minutes before ischemia(group II), Amifostine 10 mg(0.2 mL) injection during ischemia through coronary artery(group III),and Amifostine 50 mg(1 mL) peritoneal injection 2 hrs before ischemia(group IV). The experimental parameters were the levels of latate, CK-MB, and adenosine deaminase(ADA) in frozen myocardium, the quantity of coronary flow,and left ventricular developed pressure, and it's dp/dt. Statistical analysis was performed using repeated measured analysis of variance and student t-test. Result: The coronary flow of group II and IV were less than group I and III at equilibrium state but recovery of coronary flow at reperfusion state of group II, III, and IV were more increased compared with group I. The change of systolic left ventricular devoloping pressure of group II and IV were less than control group at equilibrium state, which seemed to be the influence of the pharmacological hypotensive effect of amifostine. But it was higher compared with group I at reperfusion state. The lactic acid contents of group II were less than control group in frozen myocardium.(Group I was 0.20 0.29 mM/g vs Group II, which was 0.10 0.11 mM/g). The quantity of CK-MB in myocardial tissue was highest in group IV (P=0.026 I: 120.0 97.8 U/L vs IV: 242.2 79.15 U/L). The adenosine deaminase contents in the coronary flow and frozen myocardium were not significantly different among each group. Conclusion: Amifostine seemed to have significant cardioprotective effect during ischemia and reperfusion injuries of myocardium.

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