Schlack W, Preckel B, Stunneck D, Thämer V
Institut für Klinische Anaesthesiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Br J Anaesth. 1998 Dec;81(6):913-9. doi: 10.1093/bja/81.6.913.
A specific action against myocardial reperfusion injury of the oxygen paradox type was recently characterized for halothane after anoxic perfusion in isolated rat hearts and isolated cardiomyocytes. In this study, we have characterized the protective effects of the clinically available inhalation anaesthetics during reperfusion after ischaemia. In isolated, isovolumically beating rat hearts perfused at a constant flow (10 ml min-1, PO2 80 kPa) and paced at 350 beat min-1, we determined left ventricular developed pressure (LVDP) and release of creatine kinase (CKR) as indices of myocardial performance and cellular injury, respectively. Seven control hearts underwent 30 min of no-flow ischaemia and 1 h of reperfusion. In the treatment groups, halothane, enflurane, isoflurane, sevoflurane or desflurane (each group n = 6) was added to the perfusion medium for the first 30 min of reperfusion at a concentration corresponding to 1.5 MAC in the rat. In the control group, cellular injury occurred at early reperfusion (peak CKR 283 (SEM 57) iu litre-1 at 10 min of reperfusion). Peak CKR to the coronary venous effluent was attenuated by all anaesthetics (halothane group 156 (45), enflurane group 134 (20), sevoflurane group 132 (20), desflurane group 159 (25) iu litre-1; each P < 0.05). Isoflurane did not differ from controls (303 (53) iu litre-1; P = 0.5). In the sevoflurane group, there was a delayed peak CKR after discontinuation of the anaesthetic at 30 min of reperfusion (260 (34) iu litre-1). Functional recovery was improved by all anaesthetics, but was seen much earlier with desflurane (LVDP 28 (3)% of baseline at 5 min reperfusion compared with halothane (6 (1)%), enflurane (11 (3)%), isoflurane (9 (6)%), sevoflurane (10 (2)%) and controls (3 (1)% of baseline)). At 30 min of reperfusion, recovery of LVDP was improved to a similar extent by all anaesthetics (halothane 30 (9)%, enflurane 36 (9)%, isoflurane 33 (5)%, sevoflurane 30 (5)%, desflurane 36 (4)% of baseline values) compared with controls (13 (5)%; each P < 0.05). All inhalation anaesthetics protected against myocardial reperfusion injury, but showed differences in attenuation of cellular injury and functional recovery. These differences may suggest different protective mechanisms.
最近，在离体大鼠心脏和离体心肌细胞进行缺氧灌注后，氟烷对氧反常型心肌再灌注损伤具有特定作用。在本研究中，我们已对临床可用的吸入麻醉剂在缺血后再灌注期间的保护作用进行了特征描述。在以恒定流量（10 ml min⁻¹，PO₂ 80 kPa）灌注且以350次/分钟起搏的离体等容跳动大鼠心脏中，我们分别测定左心室舒张末压（LVDP）和肌酸激酶（CKR）释放，作为心肌功能和细胞损伤的指标。7个对照心脏经历30分钟无血流缺血和1小时再灌注。在治疗组中，在再灌注的前30分钟，将氟烷、恩氟烷、异氟烷、七氟烷或地氟烷（每组n = 6）以相当于大鼠1.5 MAC的浓度添加到灌注培养基中。在对照组中，早期再灌注时发生细胞损伤（再灌注10分钟时CKR峰值为283（标准误57）iu/L）。所有麻醉剂均使冠状静脉流出液中的CKR峰值降低（氟烷组156（45），恩氟烷组134（20），七氟烷组132（20），地氟烷组159（25）iu/L；每组P < 0.05）。异氟烷与对照组无差异（303（53）iu/L；P = 0.5）。在七氟烷组中，再灌注30分钟停止麻醉后出现CKR延迟峰值（260（34）iu/L）。所有麻醉剂均改善了功能恢复，但地氟烷出现得更早（再灌注5分钟时LVDP为基线的28（3）%，而氟烷为（6（1）%），恩氟烷为（11（3）%），异氟烷为（9（6）%），七氟烷为（10（2）%），对照组为（3（1）%）。在再灌注30分钟时，所有麻醉剂使LVDP恢复到相似程度（氟烷为基线值的30（9）%，恩氟烷为36（9）%，异氟烷为33（5）%，七氟烷为30（5）%，地氟烷为36（4）%），与对照组（13（5）%）相比（每组P < 0.05）。所有吸入麻醉剂均能预防心肌再灌注损伤，但在细胞损伤减轻和功能恢复方面存在差异。这些差异可能提示不同的保护机制。
