Applegate R J, Little W C
Department of Internal Medicine (Section of Cardiology), Bowman Gray School of Medicine, Winston-Salem, NC 27157.
Cardiovasc Res. 1994 Jul;28(7):1042-8. doi: 10.1093/cvr/28.7.1042.
Since portions of autonomic nerves and receptors are located superficially on the heart, it is possible that neuromodulatory substances in pericardial fluid may modulate cardiac contractile function by altering autonomic neurotransmission. The aim of the study was to examine this hypothesis in anaesthetised dogs instrumented to measure left ventricular pressure and volume (conductance catheter).
The effects of electrical stimulation of cardiac sympathetic efferents in the ansa subclavia (n = 6), or parasympathetic efferents in the vagus (n = 6), on left ventricular contractility were evaluated during epicardial superfusion with Tyrode solution, or Tyrode solution containing hexamethonium (1 x 10(-4) M), or procaine (2%). The slope of the end systolic pressure-volume relationship (Ees), a load independent measure of left ventricular contractility, and the position of the relationship (Vmid) were obtained by rapid transient vena caval occlusion.
Ansa subclavia stimulation increased Ees from 4.8(SD 1.8) to 8.3(3.0) mm Hg.ml-1 (p < 0.05), and Vmid shifted to the left, from 9(10) to 0(16) ml (p < 0.05). This response was abolished by epicardial superfusion with procaine, but not with hexamethonium. Vagal stimulation decreased Ees from 13.3(7.4) to 6.3(4.2) mm Hg.ml-1 (p < 0.05) and Vmid shifted to the right, from 12(10) to 18(8) ml (p < 0.05). These changes were abolished by both procaine and hexamethonium. Procaine did not affect the positive inotropic response to intravenous noradrenaline nor the cardiac depressor response to intravenous methylcholine, indicating that the myocardial contractile response was intact during epicardial superfusion with procaine.
Neuromodulatory substances in the pericardial space may alter left ventricular contractility by modifying cardiac efferent autonomic neurotransmission on the epicardial surface of the heart.
由于部分自主神经和受体位于心脏表面，心包液中的神经调节物质有可能通过改变自主神经传递来调节心脏收缩功能。本研究的目的是在植入测量左心室压力和容积（传导导管）的麻醉犬身上验证这一假设。
在用台氏液、含六甲铵（1×10⁻⁴M）的台氏液或2%普鲁卡因进行心外膜灌注期间，评估刺激锁骨下袢中的心脏交感传出神经（n = 6）或迷走神经中的副交感传出神经（n = 6）对左心室收缩力的影响。通过快速短暂的腔静脉闭塞获得收缩末期压力-容积关系（Ees）的斜率，这是一种与负荷无关的左心室收缩力测量指标，以及该关系的位置（Vmid）。
刺激锁骨下袢使Ees从4.8（标准差1.8）增加到8.3（3.0）mmHg·ml⁻¹（p < 0.05），Vmid向左移位，从9（10）ml变为0（16）ml（p < 0.05）。心外膜灌注普鲁卡因可消除这种反应，但六甲铵不能。刺激迷走神经使Ees从13.3（7.4）降低到6.3（4.2）mmHg·ml⁻¹（p < 0.05），Vmid向右移位，从12（10）ml变为18（8）ml（p < 0.05）。普鲁卡因和六甲铵均可消除这些变化。普鲁卡因不影响对静脉注射去甲肾上腺素的正性肌力反应，也不影响对静脉注射乙酰甲胆碱的心脏抑制反应，表明在心外膜灌注普鲁卡因期间心肌收缩反应完好。
心包间隙中的神经调节物质可能通过改变心脏心外膜表面的自主传出神经传递来改变左心室收缩力。
