Rydvall A, Häggmark S, Nyhman H, Reiz S
Acta Anaesthesiol Scand. 1984 Dec;28(6):690-5. doi: 10.1111/j.1399-6576.1984.tb02146.x.
The effects of enflurane with and without nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease. Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC enflurane-nitrogen-oxygen (70/30) to 1MAC enflurane-nitrous oxide-oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%). Enflurane-nitrogen-oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During enflurane-nitrous oxide-oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during enflurane-nitrogen. During enflurane-nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with nitrous oxide. It is concluded that enflurane is a powerful coronary vasodilator and in this respect slightly less potent than isoflurane. Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing hypotension. Nitrous oxide added to enflurane depresses cardiac function and augments the coronary vasodilatory effect of enflurane to a level at which coronary blood flow becomes totally pressure dependent.
在11例患有全身性动脉粥样硬化疾病的患者中，研究了有或没有氧化亚氮的恩氟烷对冠状动脉血流动力学和心肌氧合的影响。恩氟烷主要通过全身血管舒张（全身血管阻力降低41%）使全身血压下降（-50%），而通过心脏功能受损（心输出量降低27%）导致血压下降的程度较小。从1MAC恩氟烷-氮气-氧气（70/30）改为1MAC恩氟烷-氧化亚氮-氧气（70/30）会使血压和心输出量进一步下降（分别为-16%和-14%）。恩氟烷-氮气-氧气使冠状动脉血流减少（-29%），灌注压降低（-47%）。冠状动脉血管阻力下降（-20%），同时心肌氧耗量和氧摄取量降低（分别为-40%和-16%）。对4例患者进行的局部冠状动脉血流测量显示血流分布不均。在恩氟烷-氧化亚氮-氧气期间，心肌氧耗量和氧摄取量进一步降低（分别为-29%和-12%），而冠状动脉血流或阻力没有变化。在恩氟烷-氮气期间，4例患者出现心肌缺血。在恩氟烷-氧化亚氮期间，之前缺血的2例患者缺血消失，2例之前未缺血的患者出现缺血。氧化亚氮消除了局部血流分布不均。得出的结论是，恩氟烷是一种强效的冠状动脉血管扩张剂，在这方面比异氟烷稍弱。恩氟烷可能通过重新分配冠状动脉血流和/或通过产生低血压来诱发心肌缺血。添加到恩氟烷中的氧化亚氮会抑制心脏功能，并将恩氟烷的冠状动脉血管扩张作用增强到冠状动脉血流完全依赖压力的水平。
