Sato M, Hoka S, Arimura H, Ono K, Yoshitake J
Department of Anesthesiology and Critical Care Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Anesth Analg. 1991 Nov;73(5):590-6. doi: 10.1213/00000539-199111000-00014.
Changes in cardiac output in response to augmenting cardiac contractility, preload, and heart rate during enflurane anesthesia were examined in 12 open-chested dogs. Cardiac contractility was assessed by the slope of the end-systolic pressure-volume relation (Emax). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) was administered to augment cardiac contractility. Autologous blood (5.0 and 10 mL/kg) was infused to increase preload. Atrial pacing was used to increase the heart rate by about 30%. Cardiac output decreased from 96 +/- 4 (0% enflurane) (mean +/- SE) to 73 +/- 5 (1.7% enflurane) and to 46 +/- 7 mL.kg-1.min-1 (3.4% enflurane), concomitantly with decreases in Emax from 6.0 +/- 1.2 (0% enflurane) to 4.5 +/- 1.2 (1.7% enflurane) and to 2.5 +/- 0.5 mm Hg/mL (3.4% enflurane). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) increased Emax from 69% +/- 7% (compared to 0% enflurane with no dobutamine) to 139% +/- 15%, 167% +/- 25%, and 183% +/- 35% at 1.7% enflurane, and from 43% +/- 8% to 78% +/- 7%, 137% +/- 20%, and 157% +/- 22% at 3.4% enflurane, respectively. The decreases in cardiac output by 1.7% and 3.4% enflurane were reversed by the intravenous administration of 3 micrograms.kg-1.min-1 of dobutamine. Cardiac output was significantly increased by administration of 10 mL/kg of autologous blood at 1.7% enflurane, but did not significantly increase at 3.4% enflurane. Increasing the heart rate did not significantly increase cardiac output at 1.7% and 3.4% enflurane. The results of this study suggest that increasing cardiac contractility is the most effective therapeutic means of reversing circulatory depression during enflurane anesthesia.
在12只开胸犬中研究了恩氟烷麻醉期间心脏收缩力、前负荷和心率增加时心输出量的变化。通过收缩末期压力-容积关系斜率（Emax）评估心脏收缩力。给予多巴酚丁胺（3、6和9微克·千克⁻¹·分钟⁻¹）以增强心脏收缩力。输注自体血（5.0和10毫升/千克）以增加前负荷。使用心房起搏使心率增加约30%。心输出量从96±4（0%恩氟烷）（平均值±标准误）降至73±5（1.7%恩氟烷）和46±7毫升·千克⁻¹·分钟⁻¹（3.4%恩氟烷），同时Emax从6.0±1.2（0%恩氟烷）降至4.5±1.2（1.7%恩氟烷）和2.5±0.5毫米汞柱/毫升（3.4%恩氟烷）。在1.7%恩氟烷时，多巴酚丁胺（3、6和9微克·千克⁻¹·分钟⁻¹）使Emax从69%±7%（与未用多巴酚丁胺的0%恩氟烷相比）增加至139%±15%、167%±25%和183%±35%，在3.4%恩氟烷时分别从43%±8%增加至78%±7%、137%±20%和157%±22%。静脉注射3微克·千克⁻¹·分钟⁻¹的多巴酚丁胺可逆转1.7%和3.4%恩氟烷引起的心输出量降低。在1.7%恩氟烷时输注10毫升/千克自体血可使心输出量显著增加，但在3.4%恩氟烷时未显著增加。在1.7%和3.4%恩氟烷时增加心率未显著增加心输出量。本研究结果表明，增加心脏收缩力是逆转恩氟烷麻醉期间循环抑制的最有效治疗手段。
