Pagel P S, Hettrick D A, Kersten J R, Tessmer J P, Lowe D, Warltier D C
Department of Anesthesiology, the Medical College of Wisconsin and the Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee 53226, USA.
Anesthesiology. 1997 Oct;87(4):952-62. doi: 10.1097/00000542-199710000-00031.
The afterload dependence of left ventricular (LV) relaxation is accentuated in the failing heart. The authors tested the hypothesis that isoflurane and halothane alter the afterload sensitivity of LV relaxation in dogs with pacing-induced cardiomyopathy.
Dogs (n = 6) were chronically instrumented for measurement of LV and aortic pressures and subendocardial segment length. Hemodynamics were recorded, and LV relaxation was evaluated with a time constant of isovolumic relaxation (tau) under control conditions and during decreases and increases in LV load produced by abrupt inferior vena caval (IVC) occlusion and phenylephrine (intravenous infusion), respectively, in the conscious state and during isoflurane and halothane anesthesia (1.5 MAC) on separate days before and after the development of pacing-induced cardiomyopathy. The slope (R) of the tau versus LV end-systolic pressure (P[es]) relation was also used to determine the afterload sensitivity of LV relaxation.
IVC occlusion and phenylephrine produced similar or less profound changes in P(es), regional end-systolic force (an index of LV afterload), and end-systolic segment length in cardiomyopathic compared with healthy dogs. However, IVC occlusion and phenylephrine caused more pronounced alterations in tau in conscious and isoflurane- and halothane-anesthetized dogs after the development of cardiomyopathy. R was also greater in cardiomyopathic compared with healthy dogs (e.g., 0.32 +/- 0.03 before pacing to 1.00 +/- 0.13 ms/mmHg in conscious dogs). No differences in the load dependence of LV relaxation were observed between the conscious and anesthetized states before and after production of LV dysfunction.
The results indicate that isoflurane and halothane do not alter the afterload dependence of LV relaxation in the normal and cardiomyopathic heart. The lack of effect of the volatile anesthetics is probably related to anesthetic-induced reductions in the resistance to LV ejection concomitant with simultaneous negative inotropic effects.
在衰竭心脏中，左心室（LV）舒张的后负荷依赖性会增强。作者检验了异氟烷和氟烷会改变起搏诱导性心肌病犬左心室舒张的后负荷敏感性这一假设。
对6只犬进行长期仪器植入，以测量左心室和主动脉压力以及心内膜下节段长度。记录血流动力学指标，并在清醒状态下以及分别在异氟烷和氟烷麻醉（1.5MAC）期间，于起搏诱导性心肌病发生前后的不同日期，通过等容舒张时间常数（tau）评估左心室舒张功能。在控制条件下以及分别通过突然阻断下腔静脉（IVC）和静脉输注去氧肾上腺素使左心室负荷降低和增加时，进行上述评估。tau与左心室收缩末期压力（P[es]）关系的斜率（R）也用于确定左心室舒张的后负荷敏感性。
与健康犬相比，IVC阻断和去氧肾上腺素在心肌病犬中引起的P(es)、区域收缩末期力（左心室后负荷指标）和收缩末期节段长度变化相似或更小。然而，在心肌病发生后，IVC阻断和去氧肾上腺素在清醒、异氟烷和氟烷麻醉的犬中引起的tau变化更为显著。与健康犬相比，心肌病犬的R也更大（例如，起搏前清醒犬为0.32±0.03，起搏后为1.00±0.13ms/mmHg）。在左心室功能障碍产生前后，清醒和麻醉状态下左心室舒张的负荷依赖性均未观察到差异。
结果表明，异氟烷和氟烷不会改变正常和心肌病心脏中左心室舒张的后负荷依赖性。挥发性麻醉药缺乏作用可能与麻醉诱导的左心室射血阻力降低以及同时出现的负性肌力作用有关。
