Zygelman M, Mérillon J P, Guiomard A, Eustigneff T, Zannier D, Gourgon R
Arch Mal Coeur Vaiss. 1981 Jun;74(6):685-94.
Verapamil inhibits calcium influx through the slow calcium canals. The coronary an haemodynamic effects of intravenous Verapamil were studied in 8 patients with chronic coronary insufficiency documented by coronary arteriography. The following measurements were made in spontaneous rhythm and during atrial pacing under basal conditions and 10 minutes after intravenous Verapamil (0.10 to 0.17 mg/kg) relayed with a continuous infusion of 5 x 10(-3) mg/Kg/mn: heart rate, cardiac output, left ventricularr pressure (Millar 5 F micromanometer), femoral artery pressure, coronary sinus flow by continuous thermodilution, oxygen and lactate concentrations in arterial and arterio-venous oxygen difference, and index of myocardial oxygen consumption and the coefficient of lactate extraction were then calculated. The coronary and haemodynamic effects of atrial pacing were similar before and after Verapamil at a given rate. Left ventricula end diastolic pressure decreased, cardiac output and total systemic resistance were unchanged, dP/dt max increased but to a lesser degree after Verapamil (P less than 0.05). Coronary arterio-venous oxygen difference decreased after Verapamil. The coronary and haemodynamic effects of Verapamil were similar in spontaneous rhythm and during atrial pacing. In spontaneous rhythm, the heart rate and left ventricular end diastolic pressure increased. In spontaneous and paced rhythm, femoral artery pressure, total systemic resistance and dP/dt max decreased. Cardiac output remained the same. Myocardial oxygen consumption decreased mainly because of a reduced coronary arterio-venous oxygen difference and because of unchanged coronary flow in spontaneous rhythm oxygen consumption seems to have a favourable effect on the myocardial energy equilibrium as shown by the increased coefficient of lactate extraction during atrial pacing after Verapamil. This study shows the negative inotropic and arterial vasodilator effects of Verapamil to be responsible for the reduced myocardial oxygen consumption. It also caused coronary artery vasodilation.
维拉帕米可抑制通过慢钙通道的钙内流。我们对8例经冠状动脉造影证实患有慢性冠状动脉供血不足的患者,研究了静脉注射维拉帕米的冠状动脉及血流动力学效应。在基础状态下的自主心律以及心房起搏时,分别于静脉注射维拉帕米(0.10至0.17毫克/千克)后持续输注5×10⁻³毫克/千克/分钟,10分钟后进行了以下测量:心率、心输出量、左心室压力(米勒5F微型压力计)、股动脉压力、通过连续热稀释法测量冠状窦血流量、动脉及动静脉氧差中的氧和乳酸浓度,随后计算心肌氧耗指数和乳酸摄取系数。在给定心率下,维拉帕米给药前后心房起搏的冠状动脉及血流动力学效应相似。左心室舒张末期压力降低,心输出量和总全身阻力不变,最大dp/dt增加,但维拉帕米给药后增加程度较小(P小于0.05)。维拉帕米给药后冠状动静脉氧差减小。维拉帕米在自主心律和心房起搏时的冠状动脉及血流动力学效应相似。在自主心律时,心率和左心室舒张末期压力升高。在自主心律和起搏心律时,股动脉压力、总全身阻力和最大dp/dt降低。心输出量保持不变。心肌氧耗降低主要是由于冠状动静脉氧差减小,且在自主心律时冠状动脉血流量不变,氧耗似乎对心肌能量平衡有有利影响,如维拉帕米给药后心房起搏时乳酸摄取系数增加所示。本研究表明,维拉帕米的负性肌力和动脉血管舒张作用是导致心肌氧耗降低的原因。它还引起冠状动脉血管舒张。