Boscan P, Paton J F
Department of Physiology, School of Medical Science, University of Bristol, Bristol, BS8 1TD, UK.
Auton Neurosci. 2001 Jan 14;86(3):170-82. doi: 10.1016/S1566-0702(00)00255-1.
We compared the cardiorespiratory reflex responses evoked by noxious stimulation of the forelimb and cornea. Due to the depressant effects of anaesthesia on visceral reflexes we compared data from an unanaesthetised decerebrate rat model--the working heart-brainstem preparation (WHBP), with the anaesthetised rat. In both experimental models stimulation of the forelimb (mechanical pinch) evoked a tachycardia (WHBP: 19 +/- 2 bpm) and a decrease in respiratory cycle length (WHBP: from 4.1 +/- 0.2 to 2.3 +/- 0.1 s). The magnitude of response in anaesthetised animals depended on anaesthetic depth. Mechanical stimulation of the cornea evoked a bradycardia (-49.2 +/- 4.8 bpm) and an increase in respiratory cycle length from 4 +/- 0.36 to 5.88 +/- 0.2 s which was only present in the WHBP. In the WHBP activation of forelimb and corneal nociceptors both elicited significant pressor effects; in anaesthetised rats there were inconsistent changes in arterial pressure. To determine a role for the nucleus of the solitary tract (NTS) in mediating nociceptive evoked responses in the WHBP, synaptic transmission was blocked reversibly following bilateral microinjections of cobalt chloride. The heart rate responses evoked from either forelimb or corneal nociceptors were attenuated by approximately 50% (P < 0.05). A similar effect was observed using isoguvacine, a GABAA receptor agonist, to hyperpolarise NTS neurones. In conclusion, activation of forelimb and corneal nociceptors evoked contrasting patterns of cardiorespiratory response in the WHBP while in the anaesthetised rat the magnitude of the cardiorespiratory response to forelimb stimulation was quantitatively dependent on anaesthetic dose. In the WHBP, NTS neurones appear important for mediating the cardiac component of the reflex response following stimulation of nociceptive reflex pathways.
我们比较了前肢和角膜的伤害性刺激所诱发的心肺反射反应。由于麻醉对内脏反射有抑制作用,我们将来自未麻醉的去大脑大鼠模型——工作心脏-脑干标本(WHBP)的数据与麻醉大鼠的数据进行了比较。在这两种实验模型中,前肢刺激(机械挤压)均诱发心动过速(WHBP:19±2次/分钟)和呼吸周期长度缩短(WHBP:从4.1±0.2秒至2.3±0.1秒)。麻醉动物的反应幅度取决于麻醉深度。角膜的机械刺激诱发心动过缓(-49.2±4.8次/分钟)和呼吸周期长度从4±0.36秒增加至5.88±0.2秒,这仅在WHBP中出现。在WHBP中,前肢和角膜伤害感受器的激活均引发显著的升压效应;在麻醉大鼠中,动脉血压变化不一致。为了确定孤束核(NTS)在介导WHBP中伤害性诱发反应的作用,在双侧微量注射氯化钴后可逆性阻断突触传递。来自前肢或角膜伤害感受器诱发的心率反应减弱了约50%(P<0.05)。使用GABAA受体激动剂异谷卡波糖使NTS神经元超极化时也观察到了类似的效果。总之,在前肢和角膜伤害感受器激活时,WHBP中诱发了不同的心肺反应模式,而在麻醉大鼠中,对前肢刺激的心肺反应幅度在数量上取决于麻醉剂量。在WHBP中,NTS神经元似乎对介导伤害性反射途径刺激后反射反应的心脏成分很重要。