Moon P F
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Am J Vet Res. 1997 Aug;58(8):868-71.
To evaluate duration and magnitude of adrenocortical function suppression after administration of etomidate to cats.
15 purpose-bred, healthy cats.
Cats were allotted to 2 groups. Anesthesia was induced with etomidate (ET, 2 mg/kg of body weight, i.v.; n = 8) or a mixture (KD, n = 7) of ketamine (5 mg/kg; i.v) and diazepam (0.25 mg/kg, i.v.). Anesthesia was maintained with halothane in all cats for 2 hours. ACTH gel (2.2 U/kg, i.m.) was administered 30 minutes after anesthesia induction. Blood samples for cortisol assay were taken before anesthesia induction (T -30), and before (T0) and at 30, 60, 120, 180, 300, and 420 minutes after ACTH administration. Anesthesia was discontinued after the T120 sample was obtained.
After anesthesia induction, median (interquartile range [Q1-Q3]) cortisol values were significantly lower in the ET group (4 [3 to 4] micrograms/dl) at T0, compared with T -30 values and with T0 values in the KD group (5 [3 to 9] micrograms/dl). After ACTH administration, cortisol values in the ET group continued to decrease two- to threefold below T -30 values and remained decreased over the 2-hour anesthesia period. After ACTH administration, cortisol values increased twofold for 2 hours in the KD group, compared with T -30 values. One hour after anesthesia recovery, cortisol values in the ET group (3 [2 to 3] micrograms/dl) remained significantly lower than values in the KD group (9 [7 to 11] micrograms/dl) and preanesthesia values. By T300, both groups had cortisol concentration near 7 micrograms/dl, similar to preanesthesia values.
Induction of anesthesia with etomidate caused suppression of adrenocortical function during 2 hours of halothane anesthesia and 1 hour of recovery in cats. Cortisol concentration did not return to baseline until after 2 additional hours.
Results from these healthy cats suggest profound suppression of important stress hormones after anesthesia induction with etomidate, use of which could put critically ill cats at further risk.
评估给猫注射依托咪酯后肾上腺皮质功能抑制的持续时间和程度。
15只专门培育的健康猫。
将猫分为2组。一组用依托咪酯（ET，2毫克/千克体重，静脉注射；n = 8）诱导麻醉，另一组用氯胺酮（5毫克/千克；静脉注射）和地西泮（0.25毫克/千克，静脉注射）的混合物（KD，n = 7）诱导麻醉。所有猫均用氟烷维持麻醉2小时。诱导麻醉30分钟后给予促肾上腺皮质激素凝胶（2.2单位/千克，肌肉注射）。在诱导麻醉前（T -30）、给予促肾上腺皮质激素前（T0）以及给予促肾上腺皮质激素后30、60、120、180、300和420分钟采集血样用于皮质醇测定。在采集T120样本后停止麻醉。
诱导麻醉后，与T -30时的值以及KD组T0时的值（5 [3至9]微克/分升）相比，ET组在T0时的皮质醇中位数（四分位间距[Q1 - Q3]）显著更低（4 [3至4]微克/分升）。给予促肾上腺皮质激素后，ET组的皮质醇值继续下降至低于T -30时的值两至三倍，并在2小时麻醉期内持续降低。给予促肾上腺皮质激素后，KD组的皮质醇值在2小时内比T -30时的值增加了两倍。麻醉恢复1小时后，ET组的皮质醇值（3 [2至3]微克/分升）仍显著低于KD组的值（9 [7至11]微克/分升）和麻醉前的值。到T300时，两组的皮质醇浓度均接近7微克/分升，与麻醉前的值相似。
用依托咪酯诱导麻醉导致猫在氟烷麻醉的2小时和恢复的1小时内肾上腺皮质功能受到抑制。皮质醇浓度直到再过2小时后才恢复到基线水平。
这些健康猫的结果表明，用依托咪酯诱导麻醉后重要应激激素受到显著抑制，使用依托咪酯可能会使重症猫面临更大风险。
