Kühn P, Probst P
Z Kardiol. 1975 Jul;64(7):616-24.
2 series of patients with angiographically proven coronary artery disease were studied under the influence of an infusion of a beta-receptor stimulating drug (heptaminole) and of kalium-magnesium-aspartate (KMA) in high (series: I: 1000 mg of heptaminole in 25 min) and low doses (series II: 200 mg of heptaminole in 25 min) of beta-receptor stimulation. The results confirm the finding that high dose beta-receptor stimulation in patients with severe coronary artery disease results in failure of the contractile mechanism of the heart with the beta-receptor angina. However, administration of KMA simultaneously with the beta-receptor stimulator seems to be able to prevent the expected decrease of lactate extraction and results in no change in lactate AVD in series I and even in an 11% increase in lactate AVD in series II. Experimental data concerning the biochemical effects of KMA suggest that its ability to provide adequate amounts of oxaloacetone and hence to improve the function of the bricarbonic acid cycle seems to be of special importance. For this action to become relevant in coronary artery disease a situation would have to be postulated, in which an additional limiting factor of oxydative metabolism would be an inadequate supply of Krebs-cycle intermediates.
对两组经血管造影证实患有冠状动脉疾病的患者进行了研究，研究在静脉输注β受体刺激药物（海普胺醇）和高剂量（第一组：25分钟内输注1000毫克海普胺醇）及低剂量（第二组：25分钟内输注200毫克海普胺醇）β受体刺激下的门冬氨酸钾镁（KMA）的影响。结果证实了以下发现：在患有严重冠状动脉疾病的患者中，高剂量β受体刺激会导致心脏收缩机制衰竭并引发β受体心绞痛。然而，在给予β受体刺激剂的同时给予KMA似乎能够防止预期的乳酸摄取减少，并且在第一组中乳酸动静脉差（AVD）没有变化，甚至在第二组中乳酸AVD增加了11%。关于KMA生化作用的实验数据表明，其提供足够量草酰丙酮从而改善三羧酸循环功能的能力似乎尤为重要。要使这一作用在冠状动脉疾病中具有相关性，必须假定存在一种情况，即氧化代谢的另一个限制因素是三羧酸循环中间产物供应不足。
