Bolter C P, Wilson S J
Department of Physiology and the Centre for Neuroscience, University of Otago, Dunedin, New Zealand.
Am J Physiol. 1999 Apr;276(4):R1112-7. doi: 10.1152/ajpregu.1999.276.4.R1112.
We have recently shown that the intrinsic rate response to an increase in right atrial pressure is augmented when cardiac muscarinic receptors are activated. This present study examines the cardiac pacemaker response to vagal stimulation at different values of right atrial pressure in isolated rat right atrium and in the rabbit heart in situ. In the rat atrium, when pressure was raised in steps from 2 to 10 mmHg, there was a progressive reduction in the response to vagal stimulation [40.5 +/- 7.2% reduction (mean +/- SE) at 8 mmHg, P < 0.01], which was independent of the level of vagal bradycardia, that persisted in the presence of the beta-adrenergic agonist isoproterenol. In barbiturate-anesthetized rabbits with cervical vagi cut and beta-adrenergic blockade, raising right atrial pressure approximately 2.5 mmHg by blood volume expansion reduced the bradycardia elicited by electrical stimulation of the peripheral end of the right vagus nerve (9.1 +/- 1.1% reduction, P < 0.0001). These results demonstrate that vagal bradycardia is modulated by the level of right atrial pressure and suggest that normally right atrial pressure may interact with cardiac vagal activity in the control of heart rate.
我们最近发现，当心脏毒蕈碱受体被激活时，右心房压力升高所引发的内在心率反应会增强。本研究检测了在离体大鼠右心房和家兔原位心脏中，不同右心房压力值下心脏起搏器对迷走神经刺激的反应。在大鼠心房中，当压力从2 mmHg逐步升至10 mmHg时，对迷走神经刺激的反应逐渐降低[8 mmHg时降低40.5±7.2%（平均值±标准误），P<0.01]，这与迷走神经介导的心动过缓程度无关，且在存在β-肾上腺素能激动剂异丙肾上腺素的情况下依然存在。在切断颈迷走神经并进行β-肾上腺素能阻断的巴比妥麻醉家兔中，通过血容量扩张使右心房压力升高约2.5 mmHg，可降低电刺激右迷走神经外周端所引发的心动过缓（降低9.1±1.1%，P<0.0001）。这些结果表明，迷走神经介导的心动过缓受右心房压力水平的调节，并提示正常情况下右心房压力可能在心率控制中与心脏迷走神经活动相互作用。
