Martin-Flores Manuel, Paré Monique D, Tomak Emily A, Corn Morgan L, Campoy Luis
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853., Department of Animal Science, College of Agriculture and Life Sciences, Cornell University, Ithaca, NY 14853.
Am J Vet Res. 2015 Apr;76(4):302-7. doi: 10.2460/ajvr.76.4.302.
To evaluate the potency of vecuronium and duration of vecuronium-induced neuromuscular blockade in dogs with centronuclear myopathy (CNM).
6 Labrador Retrievers with autosomal-recessive CNM and 5 age- and weight-matched control dogs.
Dogs were anesthetized on 2 occasions (1-week interval) with propofol, dexmedetomidine, and isoflurane. Neuromuscular function was monitored with acceleromyography and train-of-four (TOF) stimulation. In an initial experiment, potency of vecuronium was evaluated by a cumulative-dose method, where 2 submaximal doses of vecuronium (10 μg/kg each) were administered IV sequentially. For the TOF's first twitch (T1), baseline twitch amplitude and maximal posttreatment depression of twitch amplitude were measured. In the second experiment, dogs received vecuronium (50 μg/kg, IV) and the time of spontaneous recovery to a TOF ratio (ie, amplitude of TOF's fourth twitch divided by amplitude of T1) ≥ 0.9 and recovery index (interval between return of T1 amplitude to 25% and 75% of baseline) were measured.
Depression of T1 after each submaximal dose of vecuronium was not different between groups. Median time to a TOF ratio ≥ 0.9 was 76.7 minutes (interquartile range [IQR; 25th to 75th percentile], 66.7 to 99.4 minutes) for dogs with CNM and 75.0 minutes (IQR, 47.8 to 96.5 minutes) for controls. Median recovery index was 18.0 minutes (IQR, 9.7 to 23.5 minutes) for dogs with CNM and 20.2 minutes (IQR, 8 to 25.1 minutes) for controls.
For the study dogs, neither potency nor duration of vecuronium-induced neuromuscular blockade was altered by CNM. Vecuronium can be used to induce neuromuscular blockade in dogs with autosomal-recessive CNM.
评估维库溴铵在患有中央核性肌病（CNM）的犬中的效能以及维库溴铵诱导的神经肌肉阻滞持续时间。
6只患有常染色体隐性CNM的拉布拉多寻回犬和5只年龄及体重匹配的对照犬。
犬只分两次（间隔1周）使用丙泊酚、右美托咪定和异氟烷进行麻醉。使用加速度肌电图和四个成串刺激（TOF）来监测神经肌肉功能。在初始实验中，通过累积剂量法评估维库溴铵的效能，即依次静脉注射2次亚最大剂量的维库溴铵（每次10μg/kg）。对于TOF的第一个肌颤搐（T1），测量基线肌颤搐幅度和治疗后肌颤搐幅度的最大下降值。在第二个实验中，犬只接受维库溴铵（50μg/kg，静脉注射），并测量自发恢复至TOF比值（即TOF的第四个肌颤搐幅度除以T1幅度）≥0.9的时间以及恢复指数（T1幅度恢复至基线的25%至75%之间的间隔时间）。
每组中每次亚最大剂量维库溴铵给药后T1的下降情况无差异。患有CNM的犬至TOF比值≥0.9的中位时间为76.7分钟（四分位间距[IQR；第25至75百分位数]，66.7至99.4分钟），对照犬为75.0分钟（IQR，47.8至96.5分钟）。患有CNM的犬的中位恢复指数为18.0分钟（IQR，9.7至23.5分钟），对照犬为20.2分钟（IQR，8至25.1分钟）。
对于本研究中的犬只，CNM既未改变维库溴铵诱导的神经肌肉阻滞的效能，也未改变其持续时间。维库溴铵可用于诱导患有常染色体隐性CNM的犬的神经肌肉阻滞。
