Fejfar Z, Vrána M, Hess L, Vránová Z, Blazek Z
Institute of Clinical and Experimental Medicine, Prague.
Czech Med. 1991;14(1):22-34.
The following results were obtained in an experimental study in the dogs in general pentobarbital anaesthesia: Lidocaine type antiarrhythmics (lidocaine, Xylocaine ASTRA, Ethmozin USSR) administered shortly before artery ligation have a pro-fibrillation effect. This effect is indirectly proportional to the ischaemic focus development. A 3rd-generation beta blocker with intrinsic sympathetic activity (celiprolol, Selectol Chemie-Linz) had the same electrostabilizing effect on the ventricles in the acute phase of ischaemia as a 1st-generation beta blocker (metipranolol, Trimepranol SPOFA). The 3rd-generation blocker, however, stopped short of provoking a drop in the heart rate invariably associated with the 1st-generation beta blocker. The analgesic fentanyl (G. Richter) in combination with benzodiazepine (m,idazolam, Dormicum Hoffmann-La Roche) inducs analgosedation. In this way the dose of the analgetic can be reduced and yet the analgesia and electrostability of the heart remain the same. Due to the lower dose of the analgesic there is a lesser decrease in the heart rate and blood pressure. Analgosedation can be discontinued by administering an antagonist-agonist of benzodiazepines (flumazenil, Anexate Hoffmann-La Roche) or an antagonist of potent analgesics (butorphanol, Beforal SPOFA) without the risk of eliminating, at the same time, the electrostabilizing effect of analgosedation on the ischaemically damaged ventricles of the heart. For the prevention of sudden coronary death due to ventricular fibrillation in the acute phase of local myocardial ischaemia we can, on the basis of our experimental results, recommend analgosedation and the use of beta blockers with intristic sympathetic action. The use of lidocaine antiarrhythmics may lead to a reduction in the electric stability of the heart ventricles the ischaemic focus is developing under a certain "critical" blood level of the antiarrhythmics.
在对处于戊巴比妥全身麻醉状态的犬类进行的一项实验研究中,获得了以下结果:在结扎动脉前不久给予利多卡因类抗心律失常药(利多卡因、阿斯特拉的赛罗卡因、苏联的乙吗噻嗪)具有促纤颤作用。这种作用与缺血灶的发展呈间接比例关系。一种具有内在交感活性的第三代β受体阻滞剂(塞利洛尔,林茨化学公司的Selectol)在缺血急性期对心室具有与第一代β受体阻滞剂(美替洛尔,斯波法公司的Trimepranol)相同的电稳定作用。然而,第三代阻滞剂并未像第一代β受体阻滞剂那样必然导致心率下降。镇痛剂芬太尼(吉里斯特公司)与苯二氮䓬类药物(咪达唑仑,霍夫曼 - 罗氏公司的多美康)联合使用可诱导镇痛镇静。通过这种方式,可以减少镇痛剂的剂量,而心脏的镇痛效果和电稳定性保持不变。由于镇痛剂剂量较低,心率和血压的下降幅度较小。通过给予苯二氮䓬类药物的拮抗 - 激动剂(氟马西尼,霍夫曼 - 罗氏公司的安易醒)或强效镇痛剂的拮抗剂(布托啡诺,斯波法公司的Beforal),可以停止镇痛镇静,同时不会消除镇痛镇静对心脏缺血受损心室的电稳定作用。基于我们的实验结果,为预防局部心肌缺血急性期因心室纤颤导致的猝死,我们推荐使用镇痛镇静以及具有内在交感作用的β受体阻滞剂。在抗心律失常药的某种“临界”血药浓度下,当缺血灶正在发展时,使用利多卡因类抗心律失常药可能会导致心室电稳定性降低。