Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog.
Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog.
复制标题
比较地氟烷、异氟烷、氟烷和安氟烷对长期接受仪器治疗的狗的全身和冠状动脉血流动力学作用。
DOI：
10.1097/00000542-199103000-00024
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发表时间：
1991
期刊：
影响因子：
8.8
通讯作者：
Warltier,DC
中科院分区：
文献类型：
--
作者：
Pagel,PS;Kampine,JP;Schmeling,WT;Warltier,DC
地氟烷的全身和冠状动脉血流动力学的影响进行了比较，异氟烷，氟烷，安氟醚在长期仪器狗。由于自主神经系统的功能可能会显着影响麻醉剂在体内的血流动力学作用，一系列的实验也进行了药物阻断的自主神经系统的存在下。在10只狗上进行了8组共80个实验，用于测量主动脉和左心室压力、左心室压力增加的峰值速率（dP/dt）、内膜下段长度、冠状动脉血流速度和心输出量。在清醒状态下以及在1.25和1.75 MAC地氟烷、异氟烷、氟烷和安氟烷下平衡30分钟后记录全身和冠状动脉血流动力学。在1.75 MAC下，地氟烷（相对于对照组的变化为+ 79+/-12%）比氟烷（相对于对照组的变化为+ 44+/-12%）或安氟烷（相对于对照组的变化为+ 44+/-9%）产生更大的心率增加。地氟烷比等麻醉浓度的异氟烷在更大程度上保持了平均动脉压。这一结果归因于与异氟烷相比，对外周血管阻力的影响较小，并且与其他挥发性麻醉剂相比，通过峰值正左心室dP/dt和50 mmHg时心室压力增加率（dP/dt 50）评价，对心肌收缩力的保护更大。地氟烷和异氟烷导致舒张期冠状动脉血流速度增加（在1.75 MAC时，与对照组相比分别增加+ 19+/-6和+ 35+/-12%），同时舒张期冠状动脉血管阻力降低（在1.75 MAC时，与对照组相比分别减少-41+/-12和-58 +/-6%）。在存在自主神经系统阻滞的情况下，地氟烷和异氟烷的作用几乎相同，但冠状血管舒张除外。自主神经系统阻滞后，异氟醚增加冠状动脉血流速度，而地氟醚没有。此外，地氟烷和异氟烷对心肌收缩力的抑制作用仍低于氟烷和安氟烷。总之，在等麻醉浓度下，地氟烷和异氟烷产生相似的血流动力学效应;然而，在不存在抑制自主神经反射的药物的情况下，地氟烷的负性肌力活性较小，动脉压降低较小。在该模型的限制范围内，地氟烷和异氟烷的冠状动脉血管扩张作用并不相似。在自主神经系统阻滞的犬中，当地氟烷产生的心率和心率-血压乘积增加被阻止时，地氟烷对冠状动脉血流速度没有影响。
The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. Systemic and coronary hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.25 and 1.75 MAC desflurane, isoflurane, halothane, and enflurane. Desflurane (+ 79+/-12% change from control) produced greater increases in heart rate than did halothane (+ 44+/-12% change from control) or enflurane (+ 44+/-9% change from control) at 1.75 MAC. Desflurane preserved mean arterial pressure to a greater degree than did equianesthetic concentrations of isoflurane. This result was attributed to a smaller effect on peripheral vascular resistance as compared to isoflurane and greater preservation of myocardial contractility as evaluated by peak positive left ventricular dP/dt and the rate of increase of ventricular pressure at 50 mmHg (dP/dt50) compared to other volatile anesthetics. Increases in diastolic coronary blood flow velocity (+ 19+/-6 and+ 35+/-12% change from control at 1.75 MAC, respectively) and concomitant decreases in diastolic coronary vascular resistance (-41+/-12 and-58+/-6% change from control at 1.75 MAC, respectively) were produced by desflurane and isoflurane. In the presence of autonomic nervous system blockade, the actions of desflurane and isoflurane were nearly identical with the exception of coronary vasodilation. After autonomic nervous system blockade, isoflurane increased coronary blood flow velocity, but desflurane did not. Furthermore, both desflurane and isoflurane continued to produce less depression of myocardial contractility than did halothane and enflurane. In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.