Hess W, Brückner J B, Johannsen H H, Patschke D, Schweichel E, Tarnow J
Anaesthesist. 1977 May;26(5):264-72.
The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.
在7只犬中研究了血管扩张剂硝普钠(NP)对药物诱发心肌抑制期间血流动力学和心肌耗氧量的影响。实验在戊双咪和N₂O/O₂(比例2:1)轻度麻醉、控制通气且β肾上腺素能阻断(1.5mg/kg普萘洛尔)后的开胸犬身上进行。给予负荷剂量及持续输注0.3mg/kg·min的戊巴比妥后,左心室最大dp/dt降至对照水平的50%,以此作为标准化的心肌抑制。然后以平均速率7μg/kg·min输注NP,使平均动脉压降至80mmHg并维持20分钟。血管扩张剂治疗使心输出量和每搏量增加了16%。由于左心室计算的收缩末期容积同时减少(19%),射血分数从38%增至46%。左心室舒张末期压力也显著降低(46%),这可能是心肌功能改善、外周血管血液蓄积(舒张末期容积减少6%、平均肺动脉压降低25%、中心静脉压降低45%表明)以及心室顺应性增加共同作用的结果。由于心室顺应性增加、前负荷和后负荷降低,作为心肌能量需求主要决定因素的心肌壁张力降低,心脏耗氧量减少了22%。心脏较小的需求由未改变的冠状动脉血流量提供。心脏动静脉氧差缩小表明冠状动脉扩张(10%)。本研究结果支持临床观察,即硝普钠可能改善心脏功能受损患者心肌氧供与需求之间的失衡比例。