Preckel B, Schlack W, Thämer V
Institut für Klinische Anaesthesiologie, Heinrich-Heine-Universität, Düsseldorf, Germany.
Anesth Analg. 1998 Dec;87(6):1221-7. doi: 10.1097/00000539-199812000-00001.
To investigate the effects of halothane, enflurane, and isoflurane on myocardial reperfusion injury after ischemic protection by cardioplegic arrest, isolated perfused rat hearts were arrested by infusion of cold HTK cardioplegic solution containing 0.015 mmol/L Ca2+ and underwent 30 min of ischemia and a subsequent 60 min of reperfusion. Left ventricular (LV) developed pressure and creatine kinase (CK) release were measured as variables of myocardial function and cellular injury, respectively. In the treatment groups (each n = 9), anesthetics were given during the first 30 min of reperfusion in a concentration equivalent to 1.5 minimum alveolar anesthetic concentration of the rat. Nine hearts underwent the protocol without anesthetics (controls). Seven hearts underwent ischemia and reperfusion without cardioplegia and anesthetics. In a second series of experiments, halothane was tested after cardioplegic arrest with a modified HTK solution containing 0.15 mmol/L Ca2+ to investigate the influence of calcium content on protective actions against reperfusion injury by halothane. LV developed pressure recovered to 59%+/-5% of baseline in controls. In the experiments with HTK solution, isoflurane and enflurane further improved functional recovery to 84% of baseline (P < 0.05), whereas halothane-treated hearts showed a functional recovery similar to that of controls. CK release was significantly reduced during early reperfusion by isoflurane and enflurane, but not by halothane. After cardioplegic arrest with the Ca2+-adjusted HTK solution, halothane significantly reduced CK release but did not further improve myocardial function. Isoflurane and enflurane given during the early reperfusion period after ischemic protection by cardioplegia offer additional protection against myocardial reperfusion injury. The protective actions of halothane depended on the calcium content of the cardioplegic solution.
Enflurane and isoflurane administered in concentrations equivalent to 1.5 minimum alveolar anesthetic concentration in rats during early reperfusion offer additional protection against myocardial reperfusion injury even after prior cardioplegic protection. Protective effects of halothane solely against cellular injury were observed only when cardioplegia contained a higher calcium concentration.
为研究氟烷、恩氟烷和异氟烷对心脏停搏缺血保护后心肌再灌注损伤的影响,将离体灌注大鼠心脏用含0.015 mmol/L Ca2+的冷HTK心脏停搏液灌注使其停搏,经历30分钟缺血及随后60分钟再灌注。分别测量左心室(LV)发展压和肌酸激酶(CK)释放作为心肌功能和细胞损伤的变量。在治疗组(每组n = 9)中,在再灌注的前30分钟给予麻醉剂,浓度相当于大鼠1.5倍最低肺泡麻醉浓度。9颗心脏在无麻醉剂情况下进行该方案(对照组)。7颗心脏在无心脏停搏液和麻醉剂情况下进行缺血和再灌注。在第二系列实验中,在用含0.15 mmol/L Ca2+的改良HTK溶液心脏停搏后测试氟烷,以研究钙含量对氟烷抗再灌注损伤保护作用的影响。对照组LV发展压恢复至基线的59%±5%。在使用HTK溶液的实验中,异氟烷和恩氟烷使功能恢复进一步改善至基线的84%(P < 0.05),而氟烷处理的心脏功能恢复与对照组相似。异氟烷和恩氟烷在再灌注早期显著降低CK释放,但氟烷未降低。在用调整钙的HTK溶液心脏停搏后,氟烷显著降低CK释放,但未进一步改善心肌功能。在心脏停搏缺血保护后的再灌注早期给予异氟烷和恩氟烷可提供额外的抗心肌再灌注损伤保护。氟烷的保护作用取决于心脏停搏液的钙含量。
在大鼠再灌注早期给予相当于1.5倍最低肺泡麻醉浓度的恩氟烷和异氟烷,即使先前有心脏停搏保护,也可提供额外的抗心肌再灌注损伤保护。仅当心脏停搏液含有较高钙浓度时,才观察到氟烷仅对细胞损伤的保护作用。