Barber M J, Mueller T M, Davies B G, Zipes D P
Circ Res. 1984 Oct;55(4):532-44. doi: 10.1161/01.res.55.4.532.
The intracardiac pathways carrying the cardiovascular reflex responses mediated by cardiac sympathetic and vagal afferent fibers were examined in this study. We investigated the response to epicardial applications of bradykinin (5 micrograms) and nicotine (50 micrograms) before and after regional epicardial applications of 85% phenol in chloralose anesthetized open-chest dogs. Bradykinin stimulated sympathetic afferents, while nicotine stimulated vagal afferents. Topical applications of phenol were used to interrupt these pathways. Before phenol encircling, bradykinin significantly increased--whereas nicotine significantly decreased--mean arterial blood pressure when applied at the same sites. After phenol, nicotine applied to all sites within and outside the phenol circle continued to decrease mean arterial pressure, whereas bradykinin applied to sites within the circle no longer increased mean arterial pressure. Removal of aortic and carotid baroreceptors did not significantly affect these responses. Painting horizontal stripes of phenol on the anterior and posterior left ventricular free wall basal to the site of bradykinin application eliminated the elevation in mean arterial pressure produced by bradykinin. Reapplication of bradykinin basal to the stripe restored its response. Phenol stripes eliminated the nicotine vasodepressor response only when the stripe was painted in the atrioventricular groove. When bradykinin and nicotine were injected via a nonocclusive intracoronary catheter, both drugs elicited an early depressor response (interrupted by vagotomy) and, in some animals a late pressor response (interrupted by stellectomy). Epicardial phenol encircling the flow distribution of the cannulated coronary artery interrupted most or all of the sympathetic afferents mediating pressor responses to bradykinin or nicotine, while leaving the depressor responses intact. The depressor responses were eliminated by applying phenol to the atrioventricular groove or by transecting the cervical vagi. These data suggest that sympathetic afferent fibers travel in the superficial subepicardium in an apex-to-base direction. Vagal afferent fibers travel deeper in the myocardium until they approach the atrioventricular groove, where they ascend to the superficial subepicardium.
本研究检测了由心脏交感神经和迷走神经传入纤维介导心血管反射反应的心脏内传导通路。我们在氯醛糖麻醉的开胸犬身上,于局部心外膜应用85%苯酚前后,研究了心外膜应用缓激肽(5微克)和尼古丁(50微克)的反应。缓激肽刺激交感神经传入纤维,而尼古丁刺激迷走神经传入纤维。局部应用苯酚用于中断这些传导通路。在苯酚环扎前,在相同部位应用缓激肽时可显著升高平均动脉血压,而应用尼古丁时则显著降低平均动脉血压。苯酚处理后,在苯酚环内外所有部位应用尼古丁仍持续降低平均动脉血压,而在环内部位应用缓激肽则不再升高平均动脉血压。去除主动脉和颈动脉压力感受器对这些反应无显著影响。在缓激肽应用部位下方的左心室前、后游离壁上涂抹水平条纹状苯酚,可消除缓激肽引起的平均动脉血压升高。在条纹下方重新应用缓激肽可恢复其反应。仅当条纹涂抹在房室沟时,苯酚条纹才可消除尼古丁的血管减压反应。当通过非阻塞性冠状动脉导管注射缓激肽和尼古丁时,两种药物均引起早期降压反应(迷走神经切断术可中断),在一些动物中还引起晚期升压反应(星状神经节切除术可中断)。环绕插管冠状动脉血流分布的心外膜苯酚环扎可中断介导对缓激肽或尼古丁升压反应的大部分或全部交感神经传入纤维,而降压反应不受影响。通过在房室沟应用苯酚或切断颈迷走神经可消除降压反应。这些数据表明,交感神经传入纤维在心外膜浅层沿心尖至心底方向走行。迷走神经传入纤维在心肌中走行更深,直至接近房室沟,然后在此处升至心外膜浅层。