Mouren S, Abdenour L, Souktani R, Coriat P
Département d'Anesthesie-Réanimation, Groupe Hospitalier Pitié-Salpétrière, Université Paris VI, France.
Anesthesiology. 1996 Dec;85(6):1378-85. doi: 10.1097/00000542-199612000-00019.
Experimental studies suggest that the new short-acting intravenous anesthetic agent eltanolone does not markedly alter hemodynamics or cardiac function. However, because its intrinsic effects on myocardial performance and coronary blood flow are not yet known, they were examined in isolated blood-perfused rabbit hearts.
Coronary blood flow, myocardial contractility, relaxation, and oxygen consumption were measured during perfusion of hearts with 0.1 to 10 micrograms/ml eltanolone (n = 7) or its vehicle (n = 7). To determine whether the cardiac effects of eltanolone are mediated by indirect sympathetic activation, the same dose-response curve was studied in another group of five hearts depleted of catecholamine with reserpine treatment.
Coronary blood flow significantly increased with 10 micrograms/ml eltanolone and significantly decreased with 10 micrograms/ ml eltanolone vehicle. At eltanolone concentrations less than 10 micrograms/ml, myocardial contractility and relaxation remained unchanged but decreased at 10 micrograms/ml. Myocardial contractility and relaxation were not affected by perfusion of eltanolone vehicle alone. In eltanolone-perfused hearts, unchanged myocardial oxygen consumption was associated with significant increases in coronary venous oxygen content and tension, but in vehicle-perfused hearts, it was associated with reduced coronary venous oxygen content and tension. In catecholamine-depleted hearts, the variations in myocardial performance and coronary blood flow induced by eltanolone were similar to those observed in intact hearts.
Eltanolone (0.1 to 3 micrograms/ml) did not alter myocardial performance or coronary blood flow in isolated blood-perfused rabbit hearts. These effects were not due to an eltanolone-induced indirect sympathetic activation. Cardiac depression and coronary vasodilatation were only observed at concentrations of eltanolone far greater than those in clinical range.
实验研究表明，新型短效静脉麻醉药艾托那龙不会显著改变血流动力学或心脏功能。然而，由于其对心肌性能和冠状动脉血流的内在影响尚不清楚，因此在离体血液灌注兔心脏中对其进行了研究。
在用0.1至10微克/毫升艾托那龙（n = 7）或其溶媒（n = 7）灌注心脏期间，测量冠状动脉血流、心肌收缩性、舒张性和氧消耗。为了确定艾托那龙的心脏效应是否由间接交感神经激活介导，在另一组用利血平处理使儿茶酚胺耗竭的五颗心脏中研究了相同的剂量反应曲线。
10微克/毫升艾托那龙使冠状动脉血流显著增加，而10微克/毫升艾托那龙溶媒使其显著减少。在艾托那龙浓度低于10微克/毫升时，心肌收缩性和舒张性保持不变，但在10微克/毫升时降低。单独灌注艾托那龙溶媒不影响心肌收缩性和舒张性。在艾托那龙灌注的心脏中，心肌氧消耗不变与冠状静脉氧含量和张力显著增加相关，但在溶媒灌注的心脏中，它与冠状静脉氧含量和张力降低相关。在儿茶酚胺耗竭的心脏中，艾托那龙引起的心肌性能和冠状动脉血流变化与在完整心脏中观察到的相似。
艾托那龙（0.1至3微克/毫升）在离体血液灌注兔心脏中不改变心肌性能或冠状动脉血流。这些效应不是由于艾托那龙诱导的间接交感神经激活。仅在艾托那龙浓度远高于临床范围时才观察到心脏抑制和冠状动脉血管舒张。
