Uchino Masahiro, Kuwahara Masayoshi, Ebukuro Susumu, Tsubone Hirokazu
Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan.
Auton Neurosci. 2006 Jul 30;128(1-2):25-36. doi: 10.1016/j.autneu.2005.12.006. Epub 2006 Feb 20.
We hypothesized that baroreceptor or chemoreceptor activation might be involved in the emetic, and prodromal cardiovascular and respiratory responses. To test this hypothesis, we induced the emetic responses by gastric distension in anesthetized Suncus murinus (house musk shrew), that had intact and absent baroreceptor and chemoreceptor afferents. Secondly, we stimulated the aortic depressor nerve (ADN) and the carotid sinus nerve (CSN) with or without gastric distension. Internal carotid artery ligation in the bifurcation area, which abolished reflex bradycardia by baroreceptor activation, and abolition of chemoreceptor reflex bradycardia and hyperventilation, by carotid body denervation, suppressed the emetic response but did not abolish it. ADN denervation, which produced no significant effects on the baroreceptor or chemoreceptor reflex bradycardia, had no effect on the emetic response, including the prodromal phase. CSN stimulation with gastric distension elicited retching accompanied by reflex bradycardia and hypotension during or just after stimulation, whereas ADN stimulation with gastric distension did not induce the cardiovascular reflex, and had no effects on the emetic response. These results indicate that carotid, rather than aortic, baroreceptor or chemoreceptor activation plays an important role in the augmentation of cardiac parasympathetic activity and the development of emetic response. In conclusion, carotid baroreceptor or chemoreceptor activation, which is non-emetic stimulation, acts as a modulator in the central mechanisms of emesis.
我们假设压力感受器或化学感受器激活可能参与呕吐以及前驱性心血管和呼吸反应。为验证这一假设，我们在麻醉的臭鼩（家麝鼩）中通过胃扩张诱导呕吐反应，该臭鼩的压力感受器和化学感受器传入神经完整或缺失。其次，我们在有或无胃扩张的情况下刺激主动脉减压神经（ADN）和颈动脉窦神经（CSN）。在分叉区域结扎颈内动脉，通过压力感受器激活消除反射性心动过缓，以及通过颈动脉体去神经支配消除化学感受器反射性心动过缓和过度通气，可抑制呕吐反应但不能消除它。ADN去神经支配对压力感受器或化学感受器反射性心动过缓无显著影响，对包括前驱期在内的呕吐反应也无影响。胃扩张时刺激CSN会在刺激期间或刚结束时引发干呕，并伴有反射性心动过缓和低血压，而胃扩张时刺激ADN不会诱发心血管反射也对呕吐反应无影响。这些结果表明，颈动脉而非主动脉的压力感受器或化学感受器激活在增强心脏副交感神经活动和呕吐反应的发生中起重要作用。总之，颈动脉压力感受器或化学感受器激活作为非呕吐性刺激，在呕吐的中枢机制中起调节作用。
