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AR-L 115用于冠状动脉疾病:具有正性肌力作用且能增强左心室泵功能而不诱发心绞痛。

AR-L 115 in coronary artery disease: positive inotropic effects and increase of left-ventricular pump function without inducing angina.

作者信息

Thormann J, Schlepper M, Kramer W

出版信息

Clin Exp Pharmacol Physiol. 1982 May-Jun;9(3):235-43. doi: 10.1111/j.1440-1681.1982.tb00801.x.

DOI:10.1111/j.1440-1681.1982.tb00801.x
PMID:7140005
Abstract
  1. AR-L 115 improves pump function in patients with advanced and fully treated congestive cardiomyopathy. Since, in spite of such beneficial responses, the energy cost involved might be detrimental when used in advanced coronary artery disease, we monitored clinical haemodynamic and ECG responses to AR-L 115 (2 mg/kg body weight, bolus) in ten patients with coronary artery disease who had developed angina pectoris and/or pathological increases in left ventricular-end diastolic pressure (LVEDP) at the end of a 1 min pacing stress test. 2. When subjected to these stress conditions again (but this time during the peak effect of AR-L 115), there was no longer evidence of ischaemic myocardial impairment, neither clinically by ECG or haemodynamically. 3. There were (average) increase of 43% in cardiac index, 16% in heart rate, 27% in stroke index, 20% in ejection fraction, 31% in VCF and 39% in dp/dt max, while LVEDP decreased to normal values as if at resting conditions. All changes were significant (P less than 0.05). 4. LV-systolic pressure and end diastolic volume (P greater than 0.05) remained the same. Thus the AR-L 115-induced improved LV-pump function was accomplished under stress conditions in the absence of evidence for myocardial ischaemia.
摘要
  1. AR-L 115可改善晚期充血性心肌病且已接受充分治疗患者的泵功能。然而,尽管有这些有益反应,但在晚期冠状动脉疾病中使用时,所涉及的能量消耗可能是有害的。我们监测了10例冠状动脉疾病患者对AR-L 115(2mg/kg体重,静脉推注)的临床血流动力学和心电图反应,这些患者在1分钟起搏应激试验结束时出现了心绞痛和/或左心室舒张末期压力(LVEDP)病理性升高。2. 再次接受这些应激条件时(但这次是在AR-L 115的峰值效应期间),不再有缺血性心肌损伤的证据,无论是通过心电图临床观察还是血流动力学观察。3. 心脏指数平均增加43%,心率增加16%,每搏指数增加27%,射血分数增加20%,心室周径缩短率增加31%,dp/dt max增加39%,而LVEDP降至正常值,仿佛处于静息状态。所有变化均具有显著性(P小于0.05)。4. 左心室收缩压和舒张末期容积保持不变(P大于0.05)。因此,AR-L 115诱导的左心室泵功能改善是在应激条件下实现的,且没有心肌缺血的证据。

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