Walley T J, Woods K L, Barnett D B
Department of Pharmacology and Therapeutics, University of Leicester, UK.
Eur J Clin Pharmacol. 1989;37(5):449-52. doi: 10.1007/BF00558122.
We have studied the possible anti-platelet effects of an intravenous formulation of nifedipine (0.75 mg as a bolus and an infusion of 1.2 mg.h-1 for 2 h), or equivalent volumes of the vehicle alone, or normal saline, in a double-blind crossover fashion in six healthy subjects. The effects of a standard oral formulation (20 mg sustained-release) compared to identical placebo were also studied in twelve other subjects. Platelet function was assessed by the addition of collagen, adenosine diphosphate, or adrenaline to whole blood followed by single platelet counting. Intravenous nifedipine had no effect on aggregation in response to any of the agonists, but oral nifedipine reduced aggregation caused by collagen by approximately 15%, despite similar plasma nifedipine concentrations after both formulations (18.5 ng.ml-1 after intravenous and 21.5 ng.ml-1 after oral administration). The lack of effect of intravenous nifedipine may be due to endothelial irritation caused by the vehicle. Intravenous nifedipine is unlikely to have a useful anti-platelet effect in patients who have acute coronary insufficiency.
我们采用双盲交叉方式，在6名健康受试者中研究了硝苯地平静脉制剂（0.75 mg推注，随后以1.2 mg·h⁻¹输注2小时）、等量的单纯溶媒或生理盐水的潜在抗血小板作用。在另外12名受试者中，还研究了标准口服制剂（20 mg缓释片）与相同安慰剂相比的效果。通过向全血中添加胶原蛋白、二磷酸腺苷或肾上腺素，然后进行单血小板计数来评估血小板功能。静脉注射硝苯地平对任何一种激动剂引起的聚集均无影响，但口服硝苯地平可使胶原蛋白引起的聚集减少约15%，尽管两种制剂后血浆硝苯地平浓度相似（静脉注射后为18.5 ng·ml⁻¹，口服给药后为21.5 ng·ml⁻¹）。静脉注射硝苯地平无作用可能是由于溶媒引起的内皮刺激。静脉注射硝苯地平在急性冠状动脉功能不全患者中不太可能产生有效的抗血小板作用。
