Vincent J L, Sarot J, Unger P, Kahn R J
J Cardiovasc Pharmacol. 1987 May;9(5):546-50. doi: 10.1097/00005344-198705000-00007.
We investigated the potential value of vasodilating therapy in critically ill patients with inappropriately low cardiac output during acute illness. In seven patients with low flow state during septic or postoperative state, sodium nitroprusside (20-100 micrograms/min) was compared with nicergoline (NIC) (0.5 to 2.5 mg/min), a new selective alpha 1-blocking agent with negative chronotropic action. Sodium nitroprusside (NP) decreased arterial pressure (from 90 +/- 5 to 68 +/- 5 mm Hg, p less than 0.01) and pulmonary artery balloon-occluded pressure from 20.3 +/- 3.1 to 15.4 +/- 2.8 mm Hg, p less than 0.01) and increased heart rate (from 110 +/- 11 to 120 +/- 13 beats/min, p less than 0.05) but failed to increase stroke volume (from 24.7 +/- 4.8 to 23.4 +/- 4.4 ml, NS). During NIC administration, a comparable decrease in systemic vascular resistance was associated with a significant increase in stroke volume (from 21.6 +/- 3.3 to 25.6 +/- 3.2 ml/m2, p less than 0.01) and cardiac output (CO) (from 2.4 +/- 0.3 to 2.7 +/- 0.3 L/min/m2, p less than 0.025), whereas the decrease in arterial pressure was less significant (from 91 +/- 8 to 84 +/- 7 mm Hg, p less than 0.05). Because NIC has no positive inotropic action, the most likely mechanism is that a baroreceptor-mediated increase in heart rate with NP was prevented by the negative chronotropic action of NIC. Both drugs adversely affected arterial blood oxygenation. By its unique property to decrease heart rate, NIC could represent a valuable vasodilating agent, especially in acute conditions.
我们研究了血管扩张疗法在急性疾病期间心输出量异常降低的危重症患者中的潜在价值。在7例处于脓毒症或术后低流量状态的患者中,比较了硝普钠(20 - 100微克/分钟)与尼麦角林(NIC)(0.5至2.5毫克/分钟),后者是一种具有负性变时作用的新型选择性α1阻滞剂。硝普钠(NP)降低了动脉压(从90±5降至68±5毫米汞柱,p<0.01)和肺动脉球囊闭塞压从20.3±3.1降至15.4±2.8毫米汞柱,p<0.01),并增加了心率(从110±11升至120±13次/分钟,p<0.05),但未能增加每搏量(从24.7±4.8降至23.4±4.4毫升,无显著性差异)。在给予尼麦角林期间,全身血管阻力的类似降低与每搏量的显著增加(从21.6±3.3升至25.6±3.2毫升/平方米,p<0.01)和心输出量(CO)(从2.4±0.3升至2.7±0.3升/分钟/平方米,p<0.025)相关,而动脉压的降低不太显著(从91±8降至84±7毫米汞柱,p<0.05)。由于尼麦角林没有正性肌力作用,最可能的机制是尼麦角林的负性变时作用阻止了NP引起的压力感受器介导的心率增加。两种药物均对动脉血氧合有不利影响。由于其降低心率的独特特性,尼麦角林可能是一种有价值的血管扩张剂,尤其是在急性情况下。