Punnen S, Urbanski R, Krieger A J, Sapru H N
Section of Neurological Surgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103.
Brain Res. 1987 Oct 6;422(2):336-46. doi: 10.1016/0006-8993(87)90941-3.
Intravenous injections of clonidine produce an initial transient increase in blood pressure followed by a long-lasting hypotension and bradycardia. The initial pressor response is due to activation of vascular alpha 1-adrenergic receptors while the hypotension and bradycardia are caused by the central actions of clonidine. Although, hypothalamus, nucleus tractus solitarius (NTS), ventrolateral medulla and the intermediolateral cell column of the thoracolumbar spinal cord (IML) have been implicated, the exact site of these actions of clonidine in the central nervous system is not established. The results of this investigation suggest that the pressor area in the ventrolateral medulla (VLPA) is the site of hypotensive and bradycardic actions of intravenously administered clonidine. This conclusion is based on the observation that microinjections of idazoxan, a specific alpha 2-adrenergic receptor blocker, into the VLPA prevented and reversed the hypotension and bradycardia despite the fact that other proposed sites of these actions (NTS, hypothalamus and IML) were intact and accessible to intravenously administered clonidine.
静脉注射可乐定最初会使血压短暂升高，随后出现持久的低血压和心动过缓。最初的升压反应是由于血管α1-肾上腺素能受体激活所致，而低血压和心动过缓则是可乐定的中枢作用引起的。虽然下丘脑、孤束核（NTS）、延髓腹外侧和胸腰段脊髓中间外侧细胞柱（IML）都被认为与这些作用有关，但可乐定在中枢神经系统中这些作用的确切部位尚未确定。本研究结果表明，延髓腹外侧加压区（VLPA）是静脉注射可乐定产生低血压和心动过缓作用的部位。这一结论基于以下观察结果：向VLPA微量注射特异性α2-肾上腺素能受体阻滞剂咪唑克生可预防和逆转低血压和心动过缓，尽管这些作用的其他假定部位（NTS、下丘脑和IML）完好无损且静脉注射可乐定可到达。
