Blatt Lauren K, Lashinger Erin S R, Laping Nicholas J, Su Xin
GlaxoSmithKline Pharmaceuticals, Department of Urology, King of Prussia, Pennsylvania, USA.
Neurourol Urodyn. 2009;28(5):442-6. doi: 10.1002/nau.20650.
We tested cardiovascular and visceromotor reflex (VMR) responses to urinary bladder distension (UBD) in urethane anesthetized rats to see if it can replicate the response pattern and the inhibition of bladder nociceptive transmission by analgesics seen in isoflurane anesthetized animals.
Female Sprague-Dawley rats under 3% isoflurane anesthesia were acutely instrumented with jugular venous, carotid arterial, and bladder cannulas for drug administration, blood pressure (BP) measurement, and bladder distension, respectively. Needle electrodes were placed directly into the abdominal musculature to measure myoelectrical activity subsequent to phasic UBD (30 sec in 3 min intervals). A cardiovascular response (pressor) and a VMR response (a contraction of abdominal and hind limb musculature) to UBD were evaluated in urethane (1.2 g/kg, i.v.) or isoflurane (1%) anesthetized rats.
Pressor and VMR responses to noxious UBD (60 mmHg) were generated under both anesthesics. The thresholds of stimulus response functions for both pressor and VMR responses were not affected by either anesthesics. However, the magnitude of the maximal pressor response was significantly reduced in urethane anesthesia. The analgesics, morphine, and mexiletine, significantly inhibited the VMR response to noxious UBD under both anesthetics, but the intensities of the inhibition from both analgesics under urethane anesthesia were much lower than under isoflurane anesthesia (ID50: 2.07 mg/kg vs. 0.88 mg/kg for morphine, >10 mg/kg vs. 0.47 mg/kg for mexiletine).
The rat urinary bladder distension model in urethane anesthetized rats demonstrates a blunted maximal pressor response and a reduced inhibition of visceral nociceptive transmission by analgesics. Neurourol. Urodynam. 28:442-446, 2009. (c) 2008 Wiley-Liss, Inc.
我们在氨基甲酸乙酯麻醉的大鼠中测试了对膀胱扩张(UBD)的心血管和内脏运动反射(VMR)反应,以观察其是否能复制在异氟烷麻醉动物中看到的反应模式以及镇痛药对膀胱伤害性传入的抑制作用。
将处于3%异氟烷麻醉下的雌性斯普拉格-道利大鼠急性植入颈静脉、颈动脉和膀胱插管,分别用于给药、测量血压(BP)和进行膀胱扩张。将针电极直接置于腹部肌肉组织中,以测量阶段性膀胱扩张(每3分钟30秒)后的肌电活动。在氨基甲酸乙酯(1.2 g/kg,静脉注射)或异氟烷(1%)麻醉的大鼠中评估对膀胱扩张的心血管反应(升压)和内脏运动反射反应(腹部和后肢肌肉组织收缩)。
在两种麻醉剂作用下均产生了对有害膀胱扩张(60 mmHg)的升压和内脏运动反射反应。升压和内脏运动反射反应的刺激反应函数阈值均不受任何一种麻醉剂的影响。然而,在氨基甲酸乙酯麻醉下,最大升压反应的幅度显著降低。镇痛药吗啡和美西律在两种麻醉剂作用下均显著抑制了对有害膀胱扩张的内脏运动反射反应,但在氨基甲酸乙酯麻醉下两种镇痛药的抑制强度均远低于异氟烷麻醉下的抑制强度(半数抑制剂量:吗啡为2.07 mg/kg对0.88 mg/kg,美西律>10 mg/kg对0.47 mg/kg)。
氨基甲酸乙酯麻醉大鼠的膀胱扩张模型显示出最大升压反应减弱以及镇痛药对内脏伤害性传入的抑制作用降低。《神经泌尿学与尿动力学》28:442 - 446,2009年。(c)2008威利 - 利斯公司。