Tsuboi M, Furukawa Y, Nakajima K, Kurogouchi F, Chiba S
Department of Pharmacology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan.
Am J Physiol Heart Circ Physiol. 2000 Sep;279(3):H1201-7. doi: 10.1152/ajpheart.2000.279.3.H1201.
Some parasympathetic ganglionic cells are located in the epicardial fat pad between the medial superior vena cava and the aortic root (SVC-Ao fat pad) of the dog. We investigated whether the ganglionic cells in the SVC-Ao fat pad control the right atrial contractile force, sinus cycle length (SCL), and atrioventricular (AV) conduction in the autonomically decentralized heart of the anesthetized dog. Stimulation of both sides of the cervical vagal complexes (CVS) decreased right atrial contractile force, increased SCL, and prolonged AV interval. Stimulation of the rate-related parasympathetic nerves to the sinoatrial (SA) node (SAPS) increased SCL and decreased atrial contractile force. Stimulation of the AV conduction-related parasympathetic nerves to the AV node prolonged AV interval. Trimethaphan, a ganglionic nicotinic receptor blocker, injected into the SVC-Ao fat pad attenuated the negative inotropic, chronotropic, and dromotropic responses to CVS by 33 approximately 37%. On the other hand, lidocaine, a sodium channel blocker, injected into the SVC-Ao fat pad almost totally inhibited the inotropic and chronotropic responses to CVS and partly inhibited the dromotropic one. Lidocaine or trimethaphan injected into the SAPS locus abolished the inotropic responses to SAPS, but it partly attenuated those to CVS, although these treatments abolished the chronotropic responses to SAPS or CVS. These results suggest that parasympathetic ganglionic cells in the SVC-Ao fat pad, differing from those in SA and AV fat pads, nonselectively control the atrial contractile force, SCL, and AV conduction partially in the dog heart.
一些副交感神经节细胞位于犬的上腔静脉内侧与主动脉根部之间的心外膜脂肪垫(上腔静脉 - 主动脉脂肪垫)中。我们研究了上腔静脉 - 主动脉脂肪垫中的神经节细胞是否控制麻醉犬自主神经去传入心脏的右心房收缩力、窦性周期长度(SCL)和房室(AV)传导。刺激双侧颈迷走神经复合体(CVS)可降低右心房收缩力,增加SCL,并延长房室间期。刺激与速率相关的副交感神经至窦房(SA)结(SAPS)可增加SCL并降低心房收缩力。刺激与房室传导相关的副交感神经至房室结可延长房室间期。注入上腔静脉 - 主动脉脂肪垫的神经节烟碱受体阻滞剂曲美芬,使对CVS的负性变力、变时和变传导反应减弱约33%至37%。另一方面,注入上腔静脉 - 主动脉脂肪垫的钠通道阻滞剂利多卡因几乎完全抑制了对CVS的变力和变时反应,并部分抑制了变传导反应。注入SAPS部位的利多卡因或曲美芬消除了对SAPS的变力反应,但部分减弱了对CVS的变力反应,尽管这些处理消除了对SAPS或CVS的变时反应。这些结果表明,上腔静脉 - 主动脉脂肪垫中的副交感神经节细胞与窦房和房室脂肪垫中的不同,在犬心脏中可非选择性地部分控制心房收缩力、SCL和房室传导。