Chan S H, Lin A M
Institute of Pharmacology, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China.
Neuropharmacology. 1988 Feb;27(2):157-62. doi: 10.1016/0028-3908(88)90165-7.
The simultaneous effects of guanabenz on the activity of single-neurons in the nucleus reticularis gigantocellularis of the medulla oblongata, systemic arterial pressure and heart rate were assessed in Sprague-Dawley rats, anesthetized with pentobarbital sodium (40 mg/kg, i.p.). Of the 35 arterial pressure-related neurons (neurons that temporally altered their spike rhythm subsequent to fluctuations in arterial pressure) which were evaluated in this reticular nucleus, 32 changed their discharge frequencies that exhibited a degree and time-course parallel to the hypotension promoted by the amino-guanidine compound (5, 10 or 20 micrograms/kg, i.v.). More importantly, these alterations neuronal activity preceded the occurrence of the induced vasodepression, signifying a causative relationship between the two events. Four of the 5 non-arterial pressure-related neurons in the gigantocellular reticular nucleus, on the other hand, manifested no basic modification in their spike frequencies in relation to the hypotension induced by guanabenz. These observations provided further support for the idea that the nucleus reticularis gigantocellularis participates actively in the cardiovascular suppressive actions of the aminoguanidine compound.
在用戊巴比妥钠（40毫克/千克，腹腔注射）麻醉的Sprague-Dawley大鼠中，评估了胍那苄对延髓巨细胞网状核单个神经元活动、体循环动脉压和心率的同时影响。在这个网状核中评估的35个与动脉压相关的神经元（即那些在动脉压波动后暂时改变其放电节律的神经元）中，有32个改变了它们的放电频率，其变化程度和时程与氨基胍化合物（5、10或20微克/千克，静脉注射）引起的低血压平行。更重要的是，这些神经元活动的改变先于诱导的血管减压的发生，这表明这两个事件之间存在因果关系。另一方面，巨细胞网状核中5个与动脉压无关的神经元中有4个，其放电频率相对于胍那苄诱导的低血压没有表现出基本变化。这些观察结果进一步支持了巨细胞网状核积极参与氨基胍化合物的心血管抑制作用这一观点。
