Bagger J P, Nielsen T T
Eur Heart J. 1985 Jan;6(1):75-84. doi: 10.1093/oxfordjournals.eurheartj.a061757.
The effect of 30 mg sublingual nifedipine on cardiac metabolism and haemodynamics was studied during two identical periods of pacing in 11 patients with chronic coronary artery disease. The pace time to angina pectoris improved after nifedipine in 6 patients, deteriorated in 2 and was unchanged in 3. Nifedipine decreased blood pressure (12%), rate pressure product (10%) and coronary vascular resistance (17%) during pacing. Aorto-coronary sinus (A-Cs) oxygen difference decreased at rest (9%) and postpacing (10%) after nifedipine, although an opposite tendency in coronary sinus blood flow resulted in unchanged myocardial oxygen uptake throughout the study. Although mean myocardial lactate extraction after nifedipine was unchanged during pacing in the whole group of patients, it increased in 9 patients who showed a net lactate release at control pacing (from -50.9 +/- 33.5% to -35.9 +/- 30.2%, P less than 0.05). Nifedipine increased free fatty acid (FFA) extraction during pacing (from 1.5 +/- 12.9% to 17.4 +/- 13.1%, P less than 0.02) and uptake (from 1.8 +/- 8.5 to 11.1 +/- 10.6 mu mol min-1, P less than 0.05). Nifedipine influenced only glucose exchange significantly (46% decreased extraction) at 5 min postpacing. The A-Cs citrate gradient lessened 30-40% postpacing after nifedipine administration. Since the unloading effects of nifedipine did not alter myocardial oxygen uptake, the most important net haemodynamic finding was the decrease in coronary vascular resistance. Although no significant antianginal effect of a fixed dose of nifedipine was found, the increased uptake of FFA may reflect improved myocardial oxidative metabolism after nifedipine.
在11例慢性冠状动脉疾病患者的两个相同起搏阶段,研究了30毫克舌下含服硝苯地平对心脏代谢和血流动力学的影响。硝苯地平治疗后,6例患者心绞痛发作的起搏时间改善,2例恶化,3例无变化。起搏期间,硝苯地平降低了血压(12%)、心率血压乘积(10%)和冠状血管阻力(17%)。硝苯地平给药后,静息时和起搏后主动脉-冠状窦(A-Cs)氧差降低(9%),尽管冠状窦血流呈相反趋势,但整个研究期间心肌氧摄取未变。虽然硝苯地平治疗后全组患者起搏期间平均心肌乳酸摄取无变化,但9例在对照起搏时出现净乳酸释放的患者中,其乳酸摄取增加(从-50.9±33.5%增至-35.9±30.2%,P<0.05)。硝苯地平使起搏期间游离脂肪酸(FFA)摄取增加(从1.5±12.9%增至17.4±13.1%,P<0.02),摄取量增加(从1.8±8.5增至11.1±10.6微摩尔/分钟,P<0.05)。硝苯地平仅在起搏后5分钟对葡萄糖交换有显著影响(摄取减少46%)。硝苯地平给药后,起搏后A-Cs柠檬酸盐梯度降低30-40%。由于硝苯地平的降压作用未改变心肌氧摄取,最重要的血流动力学净发现是冠状血管阻力降低。虽然未发现固定剂量硝苯地平有显著的抗心绞痛作用,但FFA摄取增加可能反映了硝苯地平治疗后心肌氧化代谢的改善。