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大鼠外侧网状核刺激的抗伤害感受与心血管效应的分离

Dissociation of antinociceptive from cardiovascular effects of stimulation in the lateral reticular nucleus in the rat.

作者信息

Janss A J, Cox B F, Brody M J, Gebhart G F

出版信息

Brain Res. 1987 Mar 3;405(1):140-9. doi: 10.1016/0006-8993(87)90998-x.

DOI:10.1016/0006-8993(87)90998-x
PMID:2882813
Abstract

The lateral reticular nucleus (LRN) in the caudal ventrolateral medulla has been implicated in the regulation of spinal nociceptive transmission and hemodynamics. Experiments were undertaken to examine the relationship between inhibition of the tail flick reflex and cardiovascular effects produced by electrical stimulation in the LRN in rats lightly anesthetized with pentobarbital. Intensity- and frequency-dependent increases in mean arterial pressure and vascular resistance in the hindquarter, mesenteric, renal and caudal arterial beds were observed. Inhibition of the tail flick reflex, however, occurred at intensities of electrical stimulation which produced no significant changes in mean arterial pressure or vascular resistance in any of the arterial beds studied. Selective stimulation of cell bodies in the LRN by microinjection of glutamate similarly inhibited the tail flick reflex but produced significant reductions in mean arterial pressure, without substantially affecting regional vascular resistances. These results suggest that the antinociceptive and depressor effects of stimulation in the LRN are mediated by activation of cell bodies, while pressor effects produced by focal electrical stimulation are mediated by activation of fibers of passage. The descending inhibition produced by stimulation in the LRN is independent of stimulation-produced cardiovascular responses.

摘要

延髓尾端腹外侧的外侧网状核(LRN)与脊髓伤害性感受传递及血流动力学调节有关。本实验旨在研究在戊巴比妥轻度麻醉的大鼠中,电刺激LRN所产生的甩尾反射抑制与心血管效应之间的关系。观察到后肢、肠系膜、肾和尾动脉床的平均动脉压和血管阻力随刺激强度和频率增加。然而,甩尾反射的抑制出现在电刺激强度下,而此强度在任何研究的动脉床中均未引起平均动脉压或血管阻力的显著变化。通过微量注射谷氨酸选择性刺激LRN中的细胞体同样抑制了甩尾反射,但导致平均动脉压显著降低,而对局部血管阻力影响不大。这些结果表明,LRN刺激的抗伤害感受和降压作用是由细胞体激活介导的,而局部电刺激产生的升压作用是由通过纤维的激活介导的。LRN刺激产生的下行抑制与刺激引起的心血管反应无关。

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