Allal J, Pornin M, Rossi F, Poupet J Y, Bordage J P, Barraine R
Arch Mal Coeur Vaiss. 1984 Apr;77(4):458-67.
The optimal dose of Captopril was evaluated by hourly haemodynamic monitoring in 10 patients with chronic congestive cardiac failure (Stage IV of the NYHA Classification) after administration of 25 mg, 50 mg, and 100 mg of Captopril. A similar improvement was observed in all the parameters considered with all three dosages. At its peak effect (90 minutes) 25 mg of Captopril caused a fall in pulmonary capillary, and mean pulmonary artery pressures, and a fall in systemic resistance of 40%, 20% and 30% respectively; with 50 mg of Captopril, the effect was a fall of 36%, 24% and 35% respectively. The cardiac index rose by 17% with 25 mg of Captopril, 28% with 50 mg and 12% with 100 mg of Captopril. Although the fall in pulmonary capillary pressure remained significant up to the 6th hour, the improvement in cardiac index was not significant after the 3rd hour. After 8 days' treatment, plasma renin activity increased from 7.01 +/- 4.68 to 23.6 +/- 18.3 ng/ml/hour (p less than 0.02) and serum aldosterone fell from 1.175 +/- 386 p. moles/l to 497 +/- 277 p. moles/l (p less than 0.001). There was no correlation between basal plasma renin activity and pre- or post-therapeutic systemic resistances. The clinical and haemodynamic improvement was sustained after 2 months' treatment in 5 of these patients without side effects. Increasing the dosage of Captopril does not reinforce or prolong its action; moderate doses (25 mg) are as effective as high doses (100 mg). Captopril, which acts by inhibiting the renin- angiotensin-aldosterone system is the current treatment of choice in severe refractory cardiac failure.
对10例慢性充血性心力衰竭(纽约心脏病协会心功能分级IV级)患者,在给予25毫克、50毫克和100毫克卡托普利后,通过每小时的血流动力学监测来评估卡托普利的最佳剂量。所有三个剂量在所有考虑的参数方面都观察到了类似的改善。在其峰值效应(90分钟)时,25毫克卡托普利导致肺毛细血管压和平均肺动脉压下降,全身阻力分别下降40%、20%和30%;50毫克卡托普利的效应是分别下降36%、24%和35%。卡托普利25毫克时心脏指数上升17%,50毫克时上升28%,100毫克时上升12%。虽然肺毛细血管压的下降在第6小时仍很显著,但心脏指数在第3小时后改善不显著。治疗8天后,血浆肾素活性从7.01±4.68增加到23.6±18.3纳克/毫升/小时(p<0.02),血清醛固酮从1.175±386皮摩尔/升降至497±277皮摩尔/升(p<0.001)。基础血浆肾素活性与治疗前或治疗后的全身阻力之间没有相关性。其中5例患者在2个月治疗后临床和血流动力学改善持续,且无副作用。增加卡托普利的剂量并不能增强或延长其作用;中等剂量(25毫克)与高剂量(100毫克)一样有效。通过抑制肾素-血管紧张素-醛固酮系统起作用的卡托普利是目前重度难治性心力衰竭的首选治疗药物。