Bloch R, Feldman J, Bousquet P, Schwartz J
Eur J Pharmacol. 1977 Sep 1;45(1):55-60. doi: 10.1016/0014-2999(77)90057-7.
The connections between the areas 'S' which have been previously described as the ventromedullary sites of the action of clonidine and the posterior hypothalamus have been investigated. Superficial electrocoagulation of the left area 'S' suppresses the pressor response to electrical stimulation of the homolateral part of the posterior hypothalamus. Although such medullary lesions cause a significant reduction of the mean arterial pressure, the contralateral hypothalamic stimulation can still increase blood pressure. Clonidine it self applied topically (8 micrograms/kg) to the ventral face of the brain stem decreases the blood pressure response to liminal hypothalamic stimulation. It is concluded that efferent pathways, which are involved in vasomotor regulation, originate in the posterior hypothalamus and run through the ventrolateral part of the brain stem. The mechanism of the blocking effect of clonidine on these pathways is discussed.
先前被描述为可乐定作用的腹侧髓质部位的“S”区与下丘脑后部之间的联系已得到研究。左侧“S”区的浅表电凝抑制了对下丘脑后部同侧部分电刺激的升压反应。尽管这种髓质损伤会导致平均动脉压显著降低,但对侧下丘脑刺激仍可使血压升高。将可乐定自身局部应用(8微克/千克)于脑干腹面可降低对阈下下丘脑刺激的血压反应。得出的结论是,参与血管运动调节的传出通路起源于下丘脑后部,并贯穿脑干的腹外侧部分。文中还讨论了可乐定对这些通路的阻断作用机制。