Raczkowska M, Eckberg D L, Ebert T J
J Auton Nerv Syst. 1983 Mar-Apr;7(3-4):271-8. doi: 10.1016/0165-1838(83)90080-2.
Respiratory sinus arrhythmia (peak-valley P-P interval changes during controlled breathing) and carotid baroreceptor-cardiac reflex responses (provoked by neck suction) were studied before and after low (0.725 microgram/kg) or high (0.043 mg/kg) dose atropine sulfate infusions in 22 healthy young adults. There was a highly significant (r = 0.78, P = 0.002) correlation between resting respiratory sinus arrhythmia and baroreflex responses. Low dose atropine increased the magnitude of sinus arrhythmia and baroreflex responses. Large dose atropine reduced sinus arrhythmia and baroreflex responses in an exponential fashion. Our results link respiratory sinus arrhythmia with baroreflex responsiveness and provide inferential evidence that vagal cardiac efferent activity is modulated by inhibitory cholinergic receptors. We speculate that blockade of these receptors by low doses of atropine amplifies vagal motoneuron responses to incoming baroreceptor information, and thereby increases average maximum and minimum levels of vagal cardiac outflow during breathing.
在22名健康年轻成年人中,研究了低剂量(0.725微克/千克)或高剂量(0.043毫克/千克)硫酸阿托品输注前后的呼吸性窦性心律失常(控制呼吸期间的峰谷P-P间期变化)和颈动脉压力感受器-心脏反射反应(通过颈部吸引诱发)。静息呼吸性窦性心律失常与压力反射反应之间存在高度显著的相关性(r = 0.78,P = 0.002)。低剂量阿托品增加了窦性心律失常和压力反射反应的幅度。大剂量阿托品以指数方式降低了窦性心律失常和压力反射反应。我们的结果将呼吸性窦性心律失常与压力反射反应性联系起来,并提供了推断性证据,表明迷走神经心脏传出活动受抑制性胆碱能受体调节。我们推测,低剂量阿托品对这些受体的阻断放大了迷走运动神经元对传入压力感受器信息的反应,从而增加了呼吸期间迷走神经心脏流出的平均最大和最小水平。