Nordlander M
Drugs. 1985;29 Suppl 2:90-101. doi: 10.2165/00003495-198500292-00018.
Short term administration of felodipine to spontaneously hypertensive rats reduced mean arterial pressure, due to peripheral vasodilatation. This vasodilatation is generalised, since blood flow, determined by the microsphere technique, is maintained or increased in most vascular beds despite substantial mean arterial blood pressure reduction. The resistance and mean arterial blood pressure reduction after felodipine was counterbalanced by an increase in cardiac output. In short term therapy, cardiac output increased because of an increase in both heart rate and stroke volume. Following long term administration of felodipine cardiac output remained elevated owing to an increase in stroke volume. The lack of tachycardia during long term felodipine administration was shown to be due to a rapid resetting of the baroreflex control of heart rate. The marked increase in stroke volume after long term administration is suggested to be due to regression of left ventricular hypertrophy and structural rebuilding of the heart towards that characteristic of the well-trained athlete. Thus, the haemodynamic pattern induced by short term felodipine administration, and probably also other antihypertensive drugs, will become modified by neurogenic and structural adaptations upon prolonged administration.
对自发性高血压大鼠短期给予非洛地平可降低平均动脉压,这是由于外周血管扩张所致。这种血管扩张是全身性的,因为尽管平均动脉血压大幅降低,但通过微球技术测定的大多数血管床的血流量仍维持不变或增加。非洛地平引起的阻力和平均动脉血压降低被心输出量增加所抵消。在短期治疗中,心输出量增加是由于心率和每搏输出量均增加。长期给予非洛地平后,由于每搏输出量增加,心输出量仍保持升高。长期给予非洛地平期间缺乏心动过速被证明是由于心率的压力反射控制快速重置所致。长期给药后每搏输出量的显著增加被认为是由于左心室肥厚的消退以及心脏结构重建为训练有素的运动员的特征。因此,短期给予非洛地平以及可能其他抗高血压药物所诱导的血流动力学模式,在长期给药后会因神经源性和结构适应性改变而发生改变。