• 제목/요약/키워드: Langendorff

검색결과 78건 처리시간 0.021초

골수단핵세포 이식에 의한 심장근육 조직 재생

  • 류주희;김일권;조승우;임상현;유경종;홍유선;최차용;김병수
    • 한국생물공학회:학술대회논문집
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    • 한국생물공학회 2003년도 생물공학의 동향(XII)
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    • pp.95-97
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    • 2003
  • 본 연구에서는 손상된 심근의 재생을 위하여 골수단핵세포를 SD 래트에 이식하였고 5주 후에 심근의 재생, 신생혈관의 형성과 더불어 심장의 기능이 향상되었음을 확인할 수 있었다. 골수단핵세포를 손상된 심근경색 부위에 넣어주는 것은 추가 보완 실험을 통하여 심근경색의 치료법으로서 이용될 수 있을 것이다.

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Chlorpromazine 이 과분극 정지심장의 재관류 손상에 미치는 보호효과 (Protective Effect of Chlorpromazine for the Isolated Rat Heart from Reperfusion Injury)

  • 류한영
    • Journal of Chest Surgery
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    • 제23권1호
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    • pp.9-15
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    • 1990
  • This study was designed to investigate the protective effect of chlorpromazine against the reperfusion injury of myocardium after high potassium cardioplegic arrest. Langendorff`s preparations of rat heart were infused with high potassium cardioplegic solution[St. Thomas Hospital Solution] at 25oC. Chlorpromazine [10-7M] increased the recovery of myocardial contractility[dp/dt], left ventricular pressure[LVP], and coronary flow rate of the reperfused heart. Both in control and experimental groups, the restoration of myocardial activity could not reach to the level of preplegic control. These results suggest that the etiologic factors of the reperfusion injury include the influence of high potassium cardioplegic solution and/or reperfusion itself, and that chlorpromazine protects myocardium from the reperfusion injury.

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Trifluoperazone 의 심근보호효과 (Myocardial Protective Effect of Trifluoperazine)

  • 류삼렬
    • Journal of Chest Surgery
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    • 제23권1호
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    • pp.1-8
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    • 1990
  • This experiment was carried out under the postulation that activation of an intracellular calcium-calmodulin complex may play an important role in myocardial injury induced by ischemia and reperfusion. Trifluoperazine[TFP], a calmodulin antagonist, was added to the potassium cardioplegic solution and used just before ischemia, and its protective effect from ischemic injury was investigated, using Langendorff rat heart model. TFP group had better post-ischemic functional recovery and lower post-ischemic contracture after 30 minutes of normothermic ischemia. Creatine kinase leakage was also decreased in TFP group but there was no statistical difference between control group and TFP group. We concluded that TFP has some protective effect from myocardial ischemic injury and its effect might be due to prevention of activation of intracellular calcium-calmodulin complex.

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흰쥐의 허혈심장에서의 Adenosine의 심근 보호 효과에 관한 연구 (Myocardial Protective Effect of Adenosine in Ischemic Rat Heart)

  • 박승규
    • Journal of Chest Surgery
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    • 제23권6호
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    • pp.1090-1106
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    • 1990
  • This study was undertaken to investigate whether adenosine administered during cardioplegic arrest could enhance myocardial protection and improve recovery of function after ischemia. Isolated Langendorff-perfused rat hearts were subjected to 40 minutes of normothermic [37oC] ischemia. Control hearts [n=10] received modified St. Thomas’ cardioplegic solution, and the remaining hearts received modified St. Thomas’ cardioplegic solution with either 20 \ulcornerM [n=10], 200 \ulcornerM [n=10] adenosine. After ischemia of 40 minutes and 30 minutes of reperfusion, left ventricular contractility was superior in all groups of adenosine-treated hearts compared with control hearts. Furthermore, there was a significant incremental increase in functional recovery with increasing dose of adenosine. Post-ischemic diastolic stiffness was significantly better in all adenosine groups compared with controls. No differences were noted in coronary flow or myocardial water content between adenosine-treated and control hearts. These data demonstrate that adenosine administered in these concentrations provides myocardial protection, preservation of myocardial ATP and creatine phosphokinase and improved post-ischemic functional hemodynamic recovery after normothermic ischemia, presumably metabolically by reducing depletion of adenosine triphosphate, inducing rapid cardiac arrest and enabling improved post-ischemic recovery.

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허혈-재관류 심근세포의 DNA에서 8-hydroxydeoxyguanosine 생성

  • 유효진;정명희;김명석;임정규
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 1993년도 제2회 신약개발 연구발표회 초록집
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    • pp.82-82
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    • 1993
  • 허혈-재관류손상 심근세포의 DNA에서 8-hydroxydeoxyguanosine (8-OHdG) 생성을 검토하였다. 흰쥐 적출심장의 Langendorff 관류 표본에서 대동맥 차단에 의한 60분 허혈후 산소가 포화된 Kredb-Henseleit용액으로 30분간 재관류 하므로서 허혈-재관류 손상을 유도하였다. 재관류 후 심근세포에서 DNA를 추출하고 HPLC(EC detector)를 이용하여 8-OHdG를 측정하였다. 실험결과 허혈-재관류 심근세포의 DNA에서 8-OHdG 함량이 증가하였으며 이는 $O_2$ 제거물질인 superoxide dismutase와 OH 제거물질인 mannitol에 의하여 방지되었다. Xanthine oxidase외 경쟁적 길항약인 allopurinol도 8-OHdG 생성을 억제하였으며 단백분해효소 억제제인 phenylsulfonylfluoride 그리고 관류액에서 칼슘의 제거 또한 허혈-재관류 심근 DNA의 생성을 방지하였다. 이상의 결과 허혈심근의 재관류시 8-OHdG 생성이 증가하며 이는 재관류 손상과 같은 산화성 심근손상을 평가하는 좋은 Index가 될 수 있을 것으로 여겨진다.

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휜쥐의 심혈관 기능에 대한 carbofuran독성작용 (carbofuran Induces Cardiovascular Dysfunction in Rat)

  • 정이숙;이수환;백은주;문창규;문창현
    • 약학회지
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    • 제45권6호
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    • pp.739-745
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    • 2001
  • Of all pesticides, carbamates are known to be most common, since alternatives such as organophosphates have long lifetime and are extremely toxic to produce a delayed neurotoxic effect. Although a number of studies about toxicity of carbofuran, a most widely used carbamate, have been reported, its cardiovascular toxicity has not yet been studied. In the present study, we investigated its cardiovascular toxic effect in anesthetized rat in vivo and in isolated Langendorff rat heart, In anesthetized rat model, carbofuran (10 mg/kg) significantly reduced heart rate, and transiently increased blood pressure. In isolated rat heart, carbofuran (10${\mu}{\textrm}{m}$) caused a significant depression in the left ventricular developed pressure (LVDP), indicating contractile dysfunction by carbofuran. Carbofuran (10${\mu}{\textrm}{m}$) also decreased coronary flow rate (CFR) in isolated heart, indicating carbofuran-induced coronary dysfunction. These results suggest that carbofuran can cause cardiac dysfunction in rat in vivo and vitro.

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DelNido 심정지액의 심근보호효과 (Evaluation of Cardioprotective Effects of DelNido Cardioplegia)

  • 우석정;장봉현;김규태
    • Journal of Chest Surgery
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    • 제33권8호
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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.

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허혈 및 재관류한 흰쥐 심장에 미치는 인삼의 영향 (Effects of Ginseng on Global Myocardial Ischemia and Reperfusion in the Rat Heart)

  • 김병채;김낙두
    • 약학회지
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    • 제32권1호
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    • pp.70-79
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    • 1988
  • The effect of Ginseng on global myocardial ischemia and reperfusion was examined in isolated perfused rat hearts. The Ginseng ethanol extract (100mg/kg/day) was administered orally for 10 days. The rat hearts were removed and perfused at 75cm $H_{2}O$ by the Langendorff method. After 25 min. of global ischemia, the hearts were reperfused. The myocardial contents of adenosine 5'-triphosphate, creatine phosphate, and calcium were assayed. There no differences in ATP levels in all group of normal and Ginseng-treated hearts. Both in non-ischemic and ischemic heart, Ginseng increased significantly tissue creatine phosphate levels compared with control. Whereas, in ischemic-reperfused heart, there was no significant difference. In the control groups, myocardial calcium contents in the ischemic hearts were decreased compared with the non-ischemic hearts. But, in the Ginseng-treated groups, the calcium contents in the ischemic herts were not changed with the nonischemic hearts. Therefore, Ginseng appears to exert its protective effect against ischemic heart condition, not against ischemic-reperfused heart condition, by regulating energy metabolism and maintaing cellular function.

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Effect of Ginseng Components on the Potassium Depleted Cardiomyopathic Rats and it's Mechanism of Action

  • Lee, Jong-Wook;Kim, Nak-Doo
    • Archives of Pharmacal Research
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    • 제8권2호
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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.

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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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