Oku S, Benson K T, Hirakawa M, Goto H
Department of Anesthesiology and Resuscitology, Okayama University, Medical School, Japan.
Anesth Analg. 1996 Sep;83(3):477-81. doi: 10.1097/00000539-199609000-00006.
To determine the effects of intravenous dexmedetomidine (DMED) on the sympathetic nervous system and to elucidate the mechanism of hypotension, we administered 3 micrograms/kg of DMED to nerve-intact and baroreceptor-denervated rabbits and compared the changes in renal sympathetic nerve activity (RSNA) and hemodynamic variables. In nerve-intact animals, mean arterial pressure (MAP) was increased briefly and then decreased significantly. Changes in RSNA were reciprocal to those of MAP. Heart rate decreased throughout the period of observation. In baroreceptor-denervated rabbits, both MAP and RSNA decreased significantly (-39.4% +/- 3.8% and -21.3% +/- 4.7%, respectively) after the initial increase of MAP. Twenty minutes after administration, hypotension had still continued (-21.1% +/- 3.2%) although RSNA returned to the baseline value. These results indicate that suppression of sympathetic nerve discharge is indeed one of the mechanisms of DMED-induced hypotension, although it may not be the principal one.
为了确定静脉注射右美托咪定(DMED)对交感神经系统的影响并阐明其导致低血压的机制,我们给完整神经和压力感受器去神经的兔子静脉注射3微克/千克的DMED,并比较肾交感神经活动(RSNA)和血流动力学变量的变化。在完整神经的动物中,平均动脉压(MAP)短暂升高,然后显著降低。RSNA的变化与MAP的变化相反。在整个观察期间心率下降。在压力感受器去神经的兔子中,MAP最初升高后,MAP和RSNA均显著降低(分别为-39.4%±3.8%和-21.3%±4.7%)。给药20分钟后,尽管RSNA恢复到基线值,但低血压仍持续存在(-21.1%±3.2%)。这些结果表明,抑制交感神经放电确实是DMED诱导低血压的机制之一,尽管它可能不是主要机制。