Saleh T M, Connell B J
Department of Anatomy and Physiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Canada.
Neuroscience. 1998 Nov;87(1):135-46. doi: 10.1016/s0306-4522(98)00149-3.
Previous investigations have provided evidence demonstrating that the extracellular release of glutamate into the parabrachial nucleus was significantly enhanced following visceral afferent activation. This period of enhanced glutamate release into the parabrachial nucleus corresponded to a time during which the pressor response to a bolus phenylephrine injection was significantly enhanced, and the reflex bradycardia was attenuated. This decrease in the sensitivity of the baroreflex is suggestive of an enhanced sympathetic tone as a result of the vagal stimulation. The present investigation was done to determine if the decreased baroreflex sensitivity observed following short-term vagal stimulation is mediated by an increase in sympathetic activity and was dependent on the parabrachial synapse. Male Sprague-Dawley rats were anaesthetized with sodium thiobutabarbitol and instrumented to monitor blood pressure and heart rate and for the placement of a stimulating electrode on the left cervical vagus nerve. Femoral arterial blood samples were taken before, during and after 2 h of vagal stimulation which were later assayed for plasma catecholamines. The results showed that plasma norepinephrine levels decreased during, and were significantly elevated immediately following termination of the vagal stimulation, indicative of an increase in sympathetic tone. To determine if the parabrachial nucleus is involved in mediating an enhanced sympathetic activity following vagal stimulation, a second group of animals underwent an identical surgical preparation, vagal stimulation and blood sampling protocol with the addition of bilateral microinjections of either the reversible anaesthetic, lidocaine, or saline into the parabrachial nucleus. The results showed that reversible blockade of the parabrachial nucleus prior to the onset of the vagal stimulation was effective in blocking both the elevation in plasma norepinephrine levels and the depressed baroreflex sensitivity previously observed following 2 h of vagal stimulation. These results suggest that the parabrachial nucleus mediated the sympathoexcitation and consequent depression in baroreflex sensitivity observed following visceral afferent activation.
先前的研究已提供证据表明，在内脏传入神经激活后，谷氨酸向臂旁核的细胞外释放显著增强。谷氨酸向臂旁核释放增强的这段时间，与对一次大剂量去氧肾上腺素注射的升压反应显著增强以及反射性心动过缓减弱的时间段相对应。压力感受性反射敏感性的降低提示迷走神经刺激导致交感神经张力增强。本研究旨在确定短期迷走神经刺激后观察到的压力感受性反射敏感性降低是否由交感神经活动增加介导，以及是否依赖于臂旁核突触。雄性Sprague-Dawley大鼠用硫喷妥钠麻醉，安装监测血压和心率的仪器，并在左颈迷走神经上放置刺激电极。在迷走神经刺激2小时前、期间和之后采集股动脉血样，随后检测血浆儿茶酚胺。结果显示，在迷走神经刺激期间血浆去甲肾上腺素水平降低，在刺激终止后立即显著升高，表明交感神经张力增加。为了确定臂旁核是否参与介导迷走神经刺激后交感神经活动增强，另一组动物接受相同的手术准备、迷走神经刺激和采血方案，同时向臂旁核双侧微量注射可逆性麻醉剂利多卡因或生理盐水。结果显示，在迷走神经刺激开始前对臂旁核进行可逆性阻断可有效阻断迷走神经刺激2小时后先前观察到的血浆去甲肾上腺素水平升高和压力感受性反射敏感性降低。这些结果表明，臂旁核介导了在内脏传入神经激活后观察到的交感神经兴奋以及随之而来的压力感受性反射敏感性降低。
