실험연구 : 허혈/재관류 시 Amiodarone이 허혈 전처치에 의한 심근보호에 미치는 영향

Background: Ischemic preconditioning (IPC) has protective effects on myocardial ischemia. These effects may be caused by ATP (adenosine triphosphate) sensitive potassium (KATP) channel activation. Amiodarone also has pharmacologic preconditioning effects, especially suppression of reperfusion arrhyt...

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Veröffentlicht in:Korean journal of anesthesiology 2006-10, Vol.51 (4), p.455
Hauptverfasser: 구은혜, Eun Hye Koo, 박중국, Chung Guk Park, 임상호, Sang Ho Lim, 박영철, Young Cheol Park
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container_issue 4
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container_title Korean journal of anesthesiology
container_volume 51
creator 구은혜
Eun Hye Koo
박중국
Chung Guk Park
임상호
Sang Ho Lim
박영철
Young Cheol Park
description Background: Ischemic preconditioning (IPC) has protective effects on myocardial ischemia. These effects may be caused by ATP (adenosine triphosphate) sensitive potassium (KATP) channel activation. Amiodarone also has pharmacologic preconditioning effects, especially suppression of reperfusion arrhythmia. The mechanisms of amiodarone effects are different from that of IPC. The aim of this study using the isolated rat working heart was 1) to confirm whether IPC and amiodarone protected against reperfusion injury; and, if so, 2) to example whether combination of IPC and amiodarone demonstrated additive effect or not. Methods: Isolated rat hearts were stabilized for 30 minutes and were subdivided into four groups. Control group was subjected low-flow ischemia of 5% dextrose water for 30 minutes. IPC group was pretreated with IPC. In Amiodarone group, whole process was same as control group except amiodarone administration during low-flow ischemia. Amiodarone-IPC group, IPC was applied and also administrated amiodarone. Isovolumetric left ventricular end systolic pressure (LVESP), left ventricular end diastolic pressure (LVEDP), dP/dtMAX and heart rate were measured. Results: Group II showed more recovered LVESP, less developed ventricular stiffness, more preserved coronary effluent flow, earlier termination of arrhythmia and smaller infarct size than Group I. Group III showed preserved LVESP and dP/dtMAX, less developed ventricular stiffness, shortest arrhythmia sustaining time, smallest infarct size among all groups. These myocardial protective effects were abolished in Group IV. Conclusions: We observed that IPC and amiodarone administration, each has myocardial protective effects against myocardial ischemia, but when they are dealt at the same time, their beneficial effects diminished. (Korean J Anesthesiol 2006; 51: 455~62)
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These effects may be caused by ATP (adenosine triphosphate) sensitive potassium (KATP) channel activation. Amiodarone also has pharmacologic preconditioning effects, especially suppression of reperfusion arrhythmia. The mechanisms of amiodarone effects are different from that of IPC. The aim of this study using the isolated rat working heart was 1) to confirm whether IPC and amiodarone protected against reperfusion injury; and, if so, 2) to example whether combination of IPC and amiodarone demonstrated additive effect or not. Methods: Isolated rat hearts were stabilized for 30 minutes and were subdivided into four groups. Control group was subjected low-flow ischemia of 5% dextrose water for 30 minutes. IPC group was pretreated with IPC. In Amiodarone group, whole process was same as control group except amiodarone administration during low-flow ischemia. Amiodarone-IPC group, IPC was applied and also administrated amiodarone. Isovolumetric left ventricular end systolic pressure (LVESP), left ventricular end diastolic pressure (LVEDP), dP/dtMAX and heart rate were measured. Results: Group II showed more recovered LVESP, less developed ventricular stiffness, more preserved coronary effluent flow, earlier termination of arrhythmia and smaller infarct size than Group I. Group III showed preserved LVESP and dP/dtMAX, less developed ventricular stiffness, shortest arrhythmia sustaining time, smallest infarct size among all groups. These myocardial protective effects were abolished in Group IV. Conclusions: We observed that IPC and amiodarone administration, each has myocardial protective effects against myocardial ischemia, but when they are dealt at the same time, their beneficial effects diminished. 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These effects may be caused by ATP (adenosine triphosphate) sensitive potassium (KATP) channel activation. Amiodarone also has pharmacologic preconditioning effects, especially suppression of reperfusion arrhythmia. The mechanisms of amiodarone effects are different from that of IPC. The aim of this study using the isolated rat working heart was 1) to confirm whether IPC and amiodarone protected against reperfusion injury; and, if so, 2) to example whether combination of IPC and amiodarone demonstrated additive effect or not. Methods: Isolated rat hearts were stabilized for 30 minutes and were subdivided into four groups. Control group was subjected low-flow ischemia of 5% dextrose water for 30 minutes. IPC group was pretreated with IPC. In Amiodarone group, whole process was same as control group except amiodarone administration during low-flow ischemia. Amiodarone-IPC group, IPC was applied and also administrated amiodarone. Isovolumetric left ventricular end systolic pressure (LVESP), left ventricular end diastolic pressure (LVEDP), dP/dtMAX and heart rate were measured. Results: Group II showed more recovered LVESP, less developed ventricular stiffness, more preserved coronary effluent flow, earlier termination of arrhythmia and smaller infarct size than Group I. Group III showed preserved LVESP and dP/dtMAX, less developed ventricular stiffness, shortest arrhythmia sustaining time, smallest infarct size among all groups. These myocardial protective effects were abolished in Group IV. Conclusions: We observed that IPC and amiodarone administration, each has myocardial protective effects against myocardial ischemia, but when they are dealt at the same time, their beneficial effects diminished. 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Isovolumetric left ventricular end systolic pressure (LVESP), left ventricular end diastolic pressure (LVEDP), dP/dtMAX and heart rate were measured. Results: Group II showed more recovered LVESP, less developed ventricular stiffness, more preserved coronary effluent flow, earlier termination of arrhythmia and smaller infarct size than Group I. Group III showed preserved LVESP and dP/dtMAX, less developed ventricular stiffness, shortest arrhythmia sustaining time, smallest infarct size among all groups. These myocardial protective effects were abolished in Group IV. Conclusions: We observed that IPC and amiodarone administration, each has myocardial protective effects against myocardial ischemia, but when they are dealt at the same time, their beneficial effects diminished. (Korean J Anesthesiol 2006; 51: 455~62)</abstract><pub>대한마취통증의학회</pub><tpages>8</tpages></addata></record>
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subjects amiodarone
ischemic preconditioning
isolated heart
myocardial protection
reperfusion arrhythmia
title 실험연구 : 허혈/재관류 시 Amiodarone이 허혈 전처치에 의한 심근보호에 미치는 영향
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