Lowe D, Hettrick D A, Pagel P S, Warltier D C
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Anesthesiology. 1996 Jul;85(1):112-20. doi: 10.1097/00000542-199607000-00016.
This investigation examined the effects of desflurane and sevoflurane on quantitative indices of left ventricular afterload derived from aortic input impedance (Zin) interpreted using a three-element Windkessel model.
After Animal Care Committee approval, dogs (n = 8) were chronically instrumented for measurement of systemic hemodynamics including aortic blood pressure and flow. On separate days, aortic pressure and flow waveforms were recorded under steady-state conditions in the conscious state and after equilibration for 30 min at 1.1, 1.3, 1.5, and 1.7 minimum alveolar concentration of desflurane or sevoflurane. Aortic input impedance spectra were obtained via power spectral analysis of aortic pressure and flow waveforms. Characteristic aortic impedance (Zc) and total arterial resistance were calculated as the mean of the magnitude of Zin between 2 and 15 Hz and the difference between Zin at zero frequency and Zc, respectively. Total arterial compliance (C) was calculated from aortic pressure and flow waveforms using the Windkessel model.
Desflurane and sevoflurane increased heart rate and decreased systolic, diastolic, and mean arterial pressure, left ventricular systolic pressure, left ventricular peak positive rate of increase in left ventricular pressure, percent segment shortening, and stroke volume. Sevoflurane, but not desflurane, decreased cardiac output. Desflurane, but not sevoflurane, decreased systemic vascular resistance. Desflurane decreased R (3,170 +/- 188 during control to 2441 +/- 220 dynes.second.centimeter-5 at 1.7 minimum alveolar concentration) and did not alter C and Zc. In contrast, sevoflurane increased C (0.57 +/- 0.05 during control to 0.79 +/- 0.05 ml/ mmHg at 1.7 minimum alveolar concentration) and Zc (139 +/- 10 during control to 194 +/- 14 dynes.second.centimeter-5 at 1.7 minimum alveolar concentration) but did not change R.
The results indicate that desflurane and sevoflurane produce substantially different effects on left ventricular afterload in chronically instrumented dogs. Desflurane-induced decreases in systemic vascular resistance occur primarily because of effects on arteriolar resistance vessels. In contrast, sevoflurane increased C and Zc concomitant with pressure-dependent reductions in aortic diameter, suggesting that this anesthetic may alter left ventricular afterload by affecting the mechanical properties of the aorta.
本研究使用三元Windkessel模型解释，探讨了地氟烷和七氟烷对源自主动脉输入阻抗（Zin）的左心室后负荷定量指标的影响。
经动物护理委员会批准后，对8只犬进行长期仪器植入，以测量包括主动脉血压和血流在内的全身血流动力学指标。在不同日期，分别在清醒状态下的稳态条件下以及在地氟烷或七氟烷的1.1、1.3、1.5和1.7最低肺泡浓度下平衡30分钟后，记录主动脉压力和血流波形。通过对主动脉压力和血流波形进行功率谱分析获得主动脉输入阻抗谱。特征性主动脉阻抗（Zc）和总动脉阻力分别计算为2至15Hz之间Zin大小的平均值以及零频率处Zin与Zc之间的差值。使用Windkessel模型根据主动脉压力和血流波形计算总动脉顺应性（C）。
地氟烷和七氟烷均使心率增加，收缩压、舒张压、平均动脉压、左心室收缩压、左心室压力上升的左心室峰值正速率、节段缩短百分比和每搏量降低。七氟烷而非地氟烷使心输出量降低。地氟烷而非七氟烷使全身血管阻力降低。地氟烷使R降低（对照期间为3170±188，在1.7最低肺泡浓度时降至2441±220达因·秒·厘米⁻⁵），且未改变C和Zc。相比之下，七氟烷使C增加（对照期间为0.57±0.05，在1.7最低肺泡浓度时升至0.79±0.05ml/mmHg）和Zc增加（对照期间为139±10，在1.7最低肺泡浓度时升至194±14达因·秒·厘米⁻⁵），但未改变R。
结果表明，地氟烷和七氟烷对长期仪器植入的犬的左心室后负荷产生显著不同的影响。地氟烷引起的全身血管阻力降低主要是由于对小动脉阻力血管的影响。相比之下，七氟烷增加C和Zc，同时伴有依赖压力的主动脉直径减小，表明这种麻醉剂可能通过影响主动脉的力学特性来改变左心室后负荷。
