Brahim J S, Thut P D
Anesth Prog. 1984 Sep-Oct;31(5):207-12.
Isoflurane is known to produce slight tachycardia in humans. This study examined the effects of isoflurane on cardiovascular parameters in dogs. Four groups, with six dogs per group, were anesthetized with isoflurane. Prior to isoflurane administration, a femoral artery catheter was inserted. Group 1 was anesthetized with isoflurane alone. Group 2 was pretreated with fentanyl prior to administration of isoflurane. Group 3, anesthetized with isoflurane alone, had a Swan-Ganz catheter introduced through the external jugular vein. Group 4 was pre-treated with fentanyl prior to administration of isoflurane, and had a Swan-Ganz catheter. Physiologic parameters were recorded at 15-min intervals as isoflurane was reduced from 3.5% to 1.5% by 0.5% increments. Heart rate increased while blood pressure decreased during induction (8.5 min) in Group 1 and then returned to control values. In Group 2, heart rate declined with no changes in blood pressure over all isoflurane concentrations. The induction time (time from initiation of the anesthetic until intubation was achieved) was 2 min. In Group 3, the heart rate increased and the blood pressure decreased, with an induction time of 10 min. Cardiac output and pulmonary artery pressure varied inversely to the isoflurane concentration. In Group 4, heart rate decreased with a minimal decrease in blood pressure, and an induction time of 3.5 min. Cardiac output and pulmonary artery pressure varied inversely to the isoflurane concentration. A fifth group of 6 dogs was monitored for heart rate only, while a mask was placed over their noses to simulate the procedure for the administration of an anesthetic. The heart rate increased similar to that of the dogs in Groups 1 and 3, but the tachycardia was abolished with the administration of fentanyl. Increased heart rate could not be directly attributed to isoflurane but was probably due to catecholamines released during induction. Fentanyl blocked this effect, resulting in a decrease in heart rate.
已知异氟烷会使人体出现轻微的心动过速。本研究检测了异氟烷对犬类心血管参数的影响。将四组实验对象,每组六只犬,用异氟烷进行麻醉。在给予异氟烷之前,插入一根股动脉导管。第一组仅用异氟烷麻醉。第二组在给予异氟烷之前先用芬太尼预处理。第三组仅用异氟烷麻醉,并通过颈外静脉插入一根 Swan-Ganz 导管。第四组在给予异氟烷之前先用芬太尼预处理,并插入一根 Swan-Ganz 导管。当异氟烷以 0.5% 的增量从 3.5% 降至 1.5% 时,每隔 15 分钟记录一次生理参数。在第一组中,诱导期(8.5 分钟)内心率增加而血压下降,然后恢复到对照值。在第二组中,在所有异氟烷浓度下,心率下降而血压无变化。诱导时间(从开始麻醉到实现插管的时间)为 2 分钟。在第三组中,心率增加且血压下降,诱导时间为 10 分钟。心输出量和肺动脉压与异氟烷浓度呈反比。在第四组中,心率下降,血压仅有轻微下降,诱导时间为 3.5 分钟。心输出量和肺动脉压与异氟烷浓度呈反比。第五组六只犬仅监测心率,同时在它们的鼻子上放置一个面罩以模拟麻醉给药过程。心率增加情况与第一组和第三组的犬相似,但给予芬太尼后心动过速被消除。心率增加不能直接归因于异氟烷,可能是由于诱导期释放的儿茶酚胺所致。芬太尼阻断了这种效应,导致心率下降。