Pagel P S, Kampine J P, Schmeling W T, Warltier D C
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Anesthesiology. 1991 May;74(5):900-7. doi: 10.1097/00000542-199105000-00016.
The direct effects of desflurane on myocardial contractility in vivo have not been characterized. Therefore, the purpose of this investigation was to systematically examine the effects of desflurane on myocardial contractile function and compare these actions to equianesthetic concentrations of isoflurane in chronically instrumented dogs. Contractility was evaluated using an established index of inotropic state, the preload recruitable stroke work (PRSW) versus end-diastolic segment length (EDL) relationship. Since autonomic nervous system tone may influence the hemodynamic effects of the volatile anesthetics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Two groups of experiments were performed with seven dogs instrumented for measurement of aortic and left ventricular pressure, the maximum rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. After autonomic nervous system blockade, ventricular pressure-segment length loops were generated using preload reduction via partial inferior vena caval occlusion. The PRSW versus EDL relation was calculated from the pressure-length loops. Dogs were then anesthetized with 1.0 or 1.5 MAC desflurane or isoflurane in a random fashion, and measurements were repeated after 30 min of equilibration at each anesthetic concentration. The PRSW versus EDL slope reflected similar changes in contractile state when desflurane or isoflurane was administered (53 +/- 4 during control to 26 +/- 4 erg.cm-2 x 10(-3).mm-1 at 1.5 MAC desflurane, and 57 +/- 5 during control to 31 +/- 3 erg.cm-2 x 10(-2).mm-1 at 1.5 MAC isoflurane). In conclusion, desflurane and isoflurane produced equivalent direct decreases in myocardial contractility.
地氟醚对体内心肌收缩力的直接影响尚未明确。因此，本研究的目的是系统地研究地氟醚对心肌收缩功能的影响，并将这些作用与慢性植入仪器的犬只中同等麻醉浓度的异氟醚的作用进行比较。使用已确立的心肌收缩状态指标，即预负荷可募集搏功（PRSW）与舒张末期节段长度（EDL）的关系来评估收缩力。由于自主神经系统张力可能会影响挥发性麻醉剂在体内的血流动力学效应，因此在自主神经系统药理学阻断的情况下进行实验。对两组共七只犬进行实验，这些犬植入了测量主动脉和左心室压力、左心室压力最大上升速率（dP/dt）、心内膜下节段长度、冠状动脉血流速度和心输出量的仪器。在自主神经系统阻断后，通过部分下腔静脉闭塞降低预负荷，生成心室压力-节段长度环。从压力-长度环计算PRSW与EDL的关系。然后以随机方式用1.0或1.5 MAC地氟醚或异氟醚麻醉犬只，在每种麻醉浓度平衡30分钟后重复测量。当给予地氟醚或异氟醚时，PRSW与EDL斜率反映了收缩状态的相似变化（对照组为53±4，在1.5 MAC地氟醚时为26±4 erg.cm-2×10(-3).mm-1，对照组为57±5，在1.5 MAC异氟醚时为31±3 erg.cm-2×10(-2).mm-1）。总之,地氟醚和异氟醚对心肌收缩力产生同等程度的直接降低作用。
