Ko Jeff C, Barletta Michele, Sen Ismail, Weil Ann B, Krimins Rebecca A, Payton Mark E, Constable Peter
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA.
J Am Vet Med Assoc. 2013 Feb 1;242(3):339-45. doi: 10.2460/javma.242.3.339.
To compare the cardiorespiratory effects of IM administration of dexmedetomidine-buprenorphine (DB) and dexmedetomidine-buprenorphine-ketamine (DBK) in dogs with subsequent reversal with atipamezole.
Prospective, randomized crossover study.
5 healthy dogs.
Dogs were instrumented for cardiac output (CO) measurement and received DB (15 μg of dexmedetomidine/kg [6.8 μg/lb] and 40 μg of buprenorphine/kg [18.2 μg/lb]) or DBK (DB plus 3 mg of ketamine/kg [1.36 mg/lb]) in randomized order while breathing room air. Atipamezole (150 μg/kg [68.2 μg/lb], IM) was administered 1 hour later. Hemodynamic data were collected in the conscious dogs and then at 5, 10, 15, 20, 30, 45, and 60 minutes after drug administration. Lactate concentration was measured in mixed venous blood samples. Oxygen delivery (Do(2)) and oxygen consumption ([Formula: see text]o(2)) were calculated.
Heart rate (HR), CO, and Do(2) decreased after DB and DBK administration. The [Formula: see text]o(2) did not change in the DB group but decreased in the DBK group. The HR was higher in the DBK group than in the DB group throughout the study, but the CO, Do(2), and [Formula: see text]o(2) values were similar for the 2 groups. Blood lactate concentrations remained low (< 1 mmol/L) throughout the study. Arterial hypoxemia and hypercapnea occurred in both groups. Mean arterial blood pressure and pulmonary artery wedge pressure were markedly increased in both groups, but to a greater extent in the DBK group. After atipamezole administration, HR, CO, and Do(2) returned to the baseline values.
Adding ketamine to the DB combination allowed dogs to maintain a higher HR and delayed the onset of sinus arrhythmias but failed to provide a significantly higher CO because of a reduction in stroke volume.
比较肌肉注射右美托咪定-丁丙诺啡(DB)和右美托咪定-丁丙诺啡-氯胺酮(DBK)对犬心肺功能的影响,随后用阿替美唑进行逆转。
前瞻性、随机交叉研究。
5只健康犬。
对犬进行心输出量(CO)测量监测,使其呼吸室内空气,随机顺序接受DB(右美托咪定15μg/kg[6.8μg/磅]和丁丙诺啡40μg/kg[18.2μg/磅])或DBK(DB加氯胺酮3mg/kg[1.36mg/磅])。1小时后肌肉注射阿替美唑(150μg/kg[68.2μg/磅])。在清醒犬中收集血流动力学数据,然后在给药后5、10、15、20、30、45和60分钟收集。在混合静脉血样本中测量乳酸浓度。计算氧输送(Do₂)和氧消耗([公式:见正文]o₂)。
给药DB和DBK后,心率(HR)、CO和Do₂降低。DB组[公式:见正文]o₂无变化,而DBK组降低。在整个研究过程中,DBK组的HR高于DB组,但两组的CO、Do₂和[公式:见正文]o₂值相似。在整个研究过程中,血乳酸浓度保持较低(<1mmol/L)。两组均出现动脉低氧血症和高碳酸血症。两组平均动脉血压和肺动脉楔压均显著升高,但DBK组升高幅度更大。给予阿替美唑后,HR、CO和Do₂恢复到基线值。
在DB组合中添加氯胺酮可使犬保持较高的HR并延迟窦性心律失常的发作,但由于每搏输出量减少,未能提供显著更高的CO。