Zurowski Daniel, Nowak Łukasz, Wordliczek Jerzy, Dobrogowski Jan, Thor Piotr J
Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland.
Folia Med Cracov. 2012;52(1-2):57-69.
Visceral pain is an important therapeutic problem. A number of studies have established that abdominal vagal afferents modulate somatic pain behavior. Although it is not clear if vagal afferents transmit nociceptive information, a change in their activity can increase or decrease nociceptive transmission in visceral pain. Aims of the present study were to determine whether the subdiaphragmatic vagus nerves play a role in the endogenous pain inhibitory mechanisms in visceral pain model and whether it involves opioidergic pathways. Data obtained in our studies show that vagus nerve plays the direct role in conveying the nociceptive information in the peritonitis model of visceral pain. We have shown, that vagal afferents exhibit an increase in excitability and subdiaphragmatic vagotomy decrease nociceptive behavior in visceral pain in rats. We have also tested two different stimulation parameters of chronic subdiaphragmatic vagal nerve stimulation: VNS1 (high-intensity) and VNS2 (low-intensity) in visceral pain model in rats. Both stimulation parameters increased pain threshold but VNS1 was more effective than VNS2. Naloxone inhibited the antinociceptive effects of VNS, reversing partially increase in the pain threshold in rats and increases number of writhes in visceral pain model. Therefore, our data indicate that this analgesic effect of the VNS is mediated, at least in part, by descending opioidergic pathways. The present study has confirmed the importance of vagal afferents for nociception in general and proven that this role is not limited to somatic pain but also extends to visceral pain.
内脏痛是一个重要的治疗难题。多项研究已证实，腹部迷走神经传入纤维可调节躯体痛行为。虽然尚不清楚迷走神经传入纤维是否传递伤害性信息，但其活动的改变可增加或减少内脏痛中的伤害性信息传递。本研究的目的是确定膈下迷走神经在内脏痛模型的内源性疼痛抑制机制中是否起作用，以及是否涉及阿片能通路。我们研究获得的数据表明，迷走神经在内脏痛腹膜炎模型中传递伤害性信息方面起直接作用。我们已经表明，迷走神经传入纤维的兴奋性增加，膈下迷走神经切断术可降低大鼠内脏痛中的伤害性行为。我们还在大鼠内脏痛模型中测试了慢性膈下迷走神经刺激的两种不同刺激参数：VNS1（高强度）和VNS2（低强度）。两种刺激参数均提高了痛阈，但VNS1比VNS2更有效。纳洛酮抑制了VNS的抗伤害性作用，部分逆转了大鼠痛阈的升高，并增加了内脏痛模型中的扭体次数。因此，我们的数据表明，VNS的这种镇痛作用至少部分是由下行阿片能通路介导的。本研究证实了迷走神经传入纤维对一般伤害感受的重要性，并证明这种作用不仅限于躯体痛，还扩展到内脏痛。
