Giancola S B, Roder S, Ciriello J
Department of Physiology, University of Western Ontario, London, Canada.
Brain Res. 1993 Mar 19;606(1):162-6. doi: 10.1016/0006-8993(93)91585-g.
The contribution of caudal ventrolateral medulla (cVLM) to the mean arterial pressure (MAP) and heart rate (HR) responses elicited by microinjections of L-glutamate (GLU) into the cardiovascular responsive region of bed nucleus of the stria terminalis (BST) was investigated in the chloralose-anesthetized, paralysed and artificially ventilated rat. Unilateral injections of GLU into BST elicited decreases in MAP of -25 +/- 3 mmHg (n = 10) and HR of -13 +/- 3 bpm (n = 10). These cardiovascular responses were not altered after a 100 nl microinjection of 0.9% NaCl into cVLM. However, the magnitudes of the decreases in MAP and HR were attenuated (-11 +/- 3 mmHg and HR, -4 +/- 1 bpm, respectively) 5 min after a 100 nl microinjection of the reversible synaptic blocker cobalt chloride (CoCl2) into cVLM. Restimulation of BST 40 min after the 100 nl microinjection of CoCl2 in cVLM elicited cardiovascular responses that were not significantly different in magnitude from those evoked before the microinjection of CoCl2 (MAP, -23 +/- 4 mmHg; HR, -12 +/- 5 bpm). In an additional series of experiments (n = 3), restimulation of BST 1 h after an ipsilateral electrolytic lesion in cVLM elicited decreases in MAP (-11 +/- 2 mmHg) and HR (-8 +/- 4 bpm) that were significantly smaller than those elicited prior to cVLM lesion. These data suggest that a component of the pathways originating in BST involved in mediating depressor responses and cardiac slowing relays in cVLM.
在水合氯醛麻醉、麻痹并人工通气的大鼠中,研究了尾侧腹外侧延髓(cVLM)对向终纹床核(BST)心血管反应区微量注射L-谷氨酸(GLU)所引发的平均动脉压(MAP)和心率(HR)反应的作用。向BST单侧注射GLU可使MAP降低-25±3 mmHg(n = 10),HR降低-13±3次/分钟(n = 10)。向cVLM微量注射100 nl 0.9%氯化钠后,这些心血管反应未发生改变。然而,向cVLM微量注射100 nl可逆性突触阻滞剂氯化钴(CoCl2)5分钟后,MAP和HR降低的幅度减弱(分别为-11±3 mmHg和HR,-4±1次/分钟)。在向cVLM微量注射CoCl2 40分钟后再次刺激BST,所引发的心血管反应在幅度上与注射CoCl2之前所引发的反应无显著差异(MAP,-23±4 mmHg;HR,-12±5次/分钟)。在另一系列实验(n = 3)中,cVLM同侧电解损伤1小时后再次刺激BST,所引发的MAP降低(-11±2 mmHg)和HR降低(-8±4次/分钟)明显小于cVLM损伤前引发的反应。这些数据表明,起源于BST的参与介导降压反应和心脏减慢的通路的一个组成部分在cVLM中中继。