Meissner A, Weber T P, Van Aken H, Zbieranek K, Rolf N
Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität, Münster, Germany.
Anesth Analg. 2000 Dec;91(6):1333-8. doi: 10.1097/00000539-200012000-00004.
Volatile anesthetics exert a protective role in myocardial ischemia. An increase in sympathetic tone might exert deleterious effects on the ischemic myocardium. The use of the volatile anesthetic desflurane in myocardial ischemia is controversial because of its sympathetic activation. We compared propofol and desflurane on myocardial stunning in chronically instrumented dogs. Mongrel dogs (n = 8) were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure, rate of rise of left ventricular pressure, and myocardial wall-thickening fraction (WTF). An occluder around the left anterior descending artery (LAD) allowed the induction of reversible LAD-ischemia. Two experiments were performed in a cross-over fashion on separate days: 1) Induction of 10 min of LAD-ischemia during desflurane anesthesia and 2) Induction of 10 min of LAD-ischemia during propofol anesthesia. Both anesthetics were discontinued immediately after completion of ischemia. WTF was measured at predetermined time points until complete recovery from ischemic dysfunction occurred. Both anesthetics caused a significant decrease of WTF in the LAD-perfused myocardium. LAD-ischemia led to a further significant decrease of LAD-WTF in both groups. During the first 3 h of reperfusion, WTF was significantly larger in the desflurane group. Mean arterial pressure and heart rate were greater during ischemia and the first 10 min of reperfusion in the desflurane group compared with the propofol group. Recovery from myocardial stunning in dogs was faster when desflurane was used at the time of ischemia as compared with propofol anesthesia. The mechanism for this difference is unclear, but sympathetic activation by desflurane was not a limiting factor for ischemic tolerance in chronically instrumented dogs.
挥发性麻醉药对心肌缺血具有保护作用。交感神经张力增加可能对缺血心肌产生有害影响。由于其交感神经激活作用,挥发性麻醉药地氟烷在心肌缺血中的应用存在争议。我们比较了丙泊酚和地氟烷对长期植入仪器的犬心肌顿抑的影响。杂种犬(n = 8)长期植入仪器以测量心率、左心房、主动脉和左心室压力、左心室压力上升速率以及心肌增厚分数(WTF)。左前降支动脉(LAD)周围的封堵器可诱导可逆性LAD缺血。在不同日期以交叉方式进行了两项实验:1)在地氟烷麻醉期间诱导10分钟的LAD缺血;2)在丙泊酚麻醉期间诱导10分钟的LAD缺血。缺血完成后立即停用两种麻醉药。在预定时间点测量WTF,直至从缺血性功能障碍完全恢复。两种麻醉药均导致LAD灌注心肌中的WTF显著降低。LAD缺血导致两组中LAD-WTF进一步显著降低。在再灌注的前3小时内,地氟烷组的WTF显著更大。与丙泊酚组相比,地氟烷组在缺血期间和再灌注的前10分钟平均动脉压和心率更高。与丙泊酚麻醉相比,在缺血时使用地氟烷时犬心肌顿抑的恢复更快。这种差异的机制尚不清楚,但地氟烷引起的交感神经激活不是长期植入仪器犬缺血耐受性的限制因素。