Boismare F, Lefrançois J
Arzneimittelforschung. 1979;29(8a):1261-6.
In 10 healthy subjects the injection of 10-methyl-1,6-diemthyl-ergoline-8 beta-methanol-(5-bromonicotinate (nicergoline, Sermion) (5 mg i.v.) caused a permanent decrease in blood pressure. This decrease in blood pressure is due to a rapidly occurring alpha-blocking effect and a secondary central alpha-stimulating effect which did not affect the postural regulating mechanisms of the arterial blood pressure in their function. The bradycardia and the elevation of the systolic volume and of the cardiac output are based on this central effect. After oral administration of 30 mg nicergoline the same modifications appeared but to a lesser extent. If nicergoline was administered in a dosage of 30 mg p.o. 1 h before bicyle exercise (100 W for 5 min), the cardiac output and blood flow in the lower extremities increased and the elevation of the systolic pressure was limited. However, the reactive tachycardia remained at the same level. The metabolic consequences of this administration resulted in an inhibited increase in the concentration of lactic acid in the blood, which is normally caused by this exertion. This favourable metabolic effect can be explained by 1. the initial bradycardia and the decrease in the total peripheral resistance whereby the oxygen consumption of the myocardium is reduced; 2. the peripheral vasodilation.
在10名健康受试者中，静脉注射10-甲基-1,6-二甲基麦角灵-8β-甲醇-（5-溴烟酸酯）（尼麦角林，喜得镇）（5毫克）导致血压持续下降。这种血压下降是由于快速出现的α阻断作用和继发性中枢α刺激作用，而这两种作用并未影响动脉血压的体位调节机制的功能。心动过缓以及收缩期血容量和心输出量的增加均基于这种中枢作用。口服30毫克尼麦角林后，也出现了相同的变化，但程度较轻。如果在自行车运动（100瓦，持续5分钟）前1小时口服30毫克尼麦角林，心输出量和下肢血流量增加，收缩压升高受到限制。然而，反应性心动过速保持在同一水平。这种给药方式的代谢结果是抑制了血液中乳酸浓度的升高，而乳酸浓度升高通常是由这种运动引起的。这种有利的代谢作用可以通过以下两点来解释：1. 最初的心动过缓和总外周阻力的降低，从而降低了心肌的氧消耗；2. 外周血管舒张。
