Weaver L C
J Auton Nerv Syst. 1981 Apr;3(2-4):253-63. doi: 10.1016/0165-1838(81)90067-9.
Afferent neurons contained within cardiac sympathetic nerves can have excitatory influences on central sympathetic outflow. The normal or pathological circumstances during which such excitatory reflexes occur are not well understood. The purpose of this research was to investigate the possibility that cardiac sympathetic afferent neurons make a significant contribution to cardiovascular control during myocardial ischemia. Afferent influences on renal nerve activity were characterized during occlusion of coronary arteries and in response to chemical stimulation of cardiac receptors by bradykinin. Reflexes were investigated in chloralose-anesthetized cats in which arterial baroreceptors had been denervated. In vagotomized cats afferent stimulation by coronary occlusion or by bradykinin caused significant increases in renal nerve activity. When vagi remained intact, coronary occlusion or epicardially applied bradykinin caused increases, decreases biphasic responses or no significant change in renal nerve activity. Thus, excitatory reflexes could be initiated by the sympathetic afferent neurons in some cats despite simultaneous vagal afferent stimulation. The responses to chemical stimulation followed the same pattern as those to coronary occlusion suggesting that a component of the afferent stimulus during ischemia may be chemical in nature. Finally, the central pathways mediating these excitatory reflexes were investigated by comparing responses to epicardially applied bradykinin in vagotomized cats prior to and following high cervical spinal cord transection or midcollicular decerebration. Excitation of renal nerve activity by this chemical afferent stimulation was reduced but still present in spinalized cats and unchanged in decerebrate cats. Thus spinal pathways may mediate at least a component of these excitatory reflexes but forebrain regions are not essential to their initiation. In summary, these findings are consistent with the contentions that: (1) cardiac sympathetic afferent neurons may initiate significant excitatory reflexes during myocardial ischemia; (2) such reflexes may be due, in part, to chemical stimulation of cardiac receptors; and (3) these reflexes can be mediated partially by spinal pathways.
心脏交感神经内的传入神经元可对中枢交感神经传出产生兴奋性影响。此类兴奋性反射发生的正常或病理情况尚未完全明了。本研究的目的是探讨心脏交感传入神经元在心肌缺血期间对心血管控制发挥重要作用的可能性。在冠状动脉闭塞期间以及对缓激肽化学刺激心脏感受器的反应中，对肾神经活动的传入影响进行了特征描述。在动脉压力感受器已去神经支配的氯醛糖麻醉猫中研究反射。在迷走神经切断的猫中，冠状动脉闭塞或缓激肽传入刺激导致肾神经活动显著增加。当迷走神经保持完整时，冠状动脉闭塞或心外膜应用缓激肽会导致肾神经活动增加、双相反应或无显著变化。因此，尽管同时存在迷走传入刺激，但在一些猫中交感传入神经元仍可引发兴奋性反射。对化学刺激的反应与冠状动脉闭塞的反应遵循相同模式，表明缺血期间传入刺激的一部分可能具有化学性质。最后，通过比较高颈段脊髓横断或中脑丘系切断前后迷走神经切断猫心外膜应用缓激肽的反应，研究了介导这些兴奋性反射的中枢通路。这种化学传入刺激引起的肾神经活动兴奋在脊髓猫中有所降低但仍然存在，而在去大脑猫中未改变。因此，脊髓通路可能至少介导了这些兴奋性反射的一部分，但前脑区域对其引发并非必不可少。总之，这些发现与以下观点一致：(1)心脏交感传入神经元可能在心肌缺血期间引发显著的兴奋性反射；(2)此类反射可能部分归因于心脏感受器的化学刺激；(3)这些反射可部分由脊髓通路介导。
