Armour J A
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, N.S., Canada.
Proc Soc Exp Biol Med. 1989 May;191(1):60-8. doi: 10.3181/00379727-191-42890.
When either substance P or vasoactive intestinal peptide was injected into an acutely decentralized intrathoracic sympathetic ganglion, short-lasting augmentation of cardiac chronotropism and inotropism was induced. These augmentations were induced before the fall in systemic arterial pressure occurred which was a consequence of these peptides leaking into the systemic circulation in enough quantity to alter peripheral vascular resistance directly. When similar volumes of normal saline were injected into an intrathoracic ganglion, no significant cardiac changes were induced. When substance P or vasoactive intestinal peptide was administered into an intrathoracic ganglion, similar cardiac augmentations were induced either before or after the intravenous administration of hexamethonium. In contrast, when these peptides were injected into an intrathoracic ganglion in which the beta-adrenergic blocking agent timolol (0.1 mg/0.1 ml of normal saline) had been administered no cardiac augmentation occurred. These data imply that in the presence of beta-adrenergic blockade intraganglionic administration of substance P or vasoactive intestinal peptide does not modify enough intrathoracic neurons to alter cardiac chronotropism and inotropism detectably. When neuropeptide Y was injected into an intrathoracic ganglion, no cardiac changes occurred. However, when cardiac augmentations were induced by sympathetic preganglionic axon stimulation these were enhanced following the intraganglionic administration of neuropeptide Y. As this effect occurred after timolol was administered into the ipsilateral ganglia, but not after intravenous administration of hexamethonium, it is proposed that the effects of neuropeptide Y are dependent upon functioning intrathoracic ganglionic nicotinic cholinergic synaptic mechanisms. Intravenous administration of either morphine or [D-ala2,D-leu5]enkephalin acetate did not alter the capacity of the preganglionic sympathetic axons to augment the heart when stimulated. Following the intravenous administration of naloxone, the positive inotropic cardiac responses induced by efferent preganglionic sympathetic axonal stimulation were enhanced minimally in control states and significantly following hexamethonium administration. Thus, it appears that enkephalins are involved in the modulation of intrathoracic ganglion neurons regulating the heart, perhaps via modification of beta-adrenergic receptors. Taken together these data indicate that substance P, vasoactive intestinal peptide, neuropeptide Y, or enkephalins modify intrathoracic ganglionic neurons which are involved in efferent sympathetic cardiac regulation.
当将P物质或血管活性肠肽注入急性去传入的胸段交感神经节时，会诱导出心脏变时性和变力性的短暂增强。这些增强作用在全身动脉压下降之前就已出现，而全身动脉压下降是这些肽大量漏入体循环从而直接改变外周血管阻力的结果。当将等量的生理盐水注入胸段神经节时，未诱导出明显的心脏变化。当将P物质或血管活性肠肽注入胸段神经节时，在静脉注射六甲铵之前或之后均诱导出类似的心脏增强作用。相反，当将这些肽注入已给予β-肾上腺素能阻滞剂噻吗洛尔（0.1mg/0.1ml生理盐水）的胸段神经节时，未出现心脏增强作用。这些数据表明，在存在β-肾上腺素能阻滞的情况下，神经节内给予P物质或血管活性肠肽不会使足够数量的胸段神经元发生改变，从而无法明显改变心脏的变时性和变力性。当将神经肽Y注入胸段神经节时，未出现心脏变化。然而，当通过交感神经节前轴突刺激诱导出心脏增强作用后，神经节内给予神经肽Y可使其增强。由于这种作用在同侧神经节给予噻吗洛尔后出现，但在静脉注射六甲铵后未出现，因此有人提出神经肽Y的作用依赖于胸段神经节烟碱型胆碱能突触机制的正常功能。静脉注射吗啡或[D-ala2,D-leu5]脑啡肽醋酸盐均未改变节前交感神经轴突在受到刺激时增强心脏功能的能力。静脉注射纳洛酮后，在对照状态下，传出节前交感神经轴突刺激诱导的正性变力性心脏反应略有增强，而在给予六甲铵后则显著增强。因此，脑啡肽似乎参与了对调节心脏的胸段神经节神经元的调制，可能是通过对β-肾上腺素能受体的修饰来实现的。综合这些数据表明，P物质、血管活性肠肽、神经肽Y或脑啡肽可改变参与传出交感神经心脏调节的胸段神经节神经元。
