Martinez E A, Hartsfield S M, Melendez L D, Matthews N S, Slater M R
Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, Texas A&M University, College Station 77843-4474, USA.
Am J Vet Res. 1997 Nov;58(11):1280-4.
To determine the cardiovascular effects of buprenorphine in isoflurane- and halothane-anesthetized dogs.
6 healthy adult hound-type dogs given buprenorphine (16 micrograms/kg of body weight, i.v.) or isovolumetric 5% dextrose solution during anesthesia with isoflurane or halothane.
Each dog was anesthetized 4 times, with a minimum of 10 days between episodes. Anesthesia was induced with isoflurane or halothane in O2 by mask, and was maintained with 1.9% isoflurane or 1.3% halothane (end-tidal concentration). The PaCO2 was maintained between 35 and 45 mm of Hg by use of mechanical ventilation, and the following variables were determined: systolic, diastolic, and mean arterial blood pressures; cardiac output; cardiac index; stroke volume; heart rate; systemic vascular resistance; mean pulmonary arterial pressure; and pulmonary vascular resistance. In addition, arterial blood samples for gas and acid-base analyses were collected at 30-minute intervals for 2.5 hours. After baseline values were recorded, dogs were randomly assigned to receive either buprenorphine (16 micrograms/kg, i.v.) or isovolumetric 5% dextrose solution. All variables were then recorded at 15-minute intervals for 2.5 hours.
During isoflurane anesthesia, buprenorphine administration caused significant (P < or = 0.05) reductions in diastolic arterial pressure, mean arterial pressure, systolic arterial pressure, cardiac index, and heart rate, whereas systemic vascular resistance increased significantly. During halothane anesthesia, buprenorphine administration caused significant decreases in heart rate, cardiac index, mean, systolic and diastolic arterial blood pressures, and stroke volume, whereas pulmonary arterial blood pressure and systemic vascular resistance increased significantly.
Although the changes seen were significant, they were not sufficiently large to be of clinical importance in healthy dogs.
确定丁丙诺啡对异氟烷和氟烷麻醉犬的心血管影响。
6只健康成年猎犬型犬,在异氟烷或氟烷麻醉期间静脉注射丁丙诺啡(16微克/千克体重)或等容5%葡萄糖溶液。
每只犬麻醉4次,每次间隔至少10天。通过面罩用异氟烷或氟烷在氧气中诱导麻醉,并用1.9%异氟烷或1.3%氟烷(呼气末浓度)维持麻醉。通过机械通气将动脉血二氧化碳分压维持在35至45毫米汞柱之间,并测定以下变量:收缩压、舒张压和平均动脉血压;心输出量;心脏指数;每搏输出量;心率;全身血管阻力;平均肺动脉压;和肺血管阻力。此外,在2.5小时内每隔30分钟采集动脉血样进行气体和酸碱分析。记录基线值后,将犬随机分为接受丁丙诺啡(16微克/千克,静脉注射)或等容5%葡萄糖溶液。然后在2.5小时内每隔15分钟记录所有变量。
在异氟烷麻醉期间,注射丁丙诺啡导致舒张压、平均动脉压、收缩压、心脏指数和心率显著降低(P≤0.05),而全身血管阻力显著增加。在氟烷麻醉期间,注射丁丙诺啡导致心率、心脏指数、平均、收缩压和舒张压以及每搏输出量显著降低,而肺动脉血压和全身血管阻力显著增加。
虽然观察到的变化显著,但在健康犬中这些变化不够大以至于具有临床重要性。