Nosaka S, Murata K, Inui K, Murase S
Department of Physiology, Mie University School of Medicine, Japan.
Pflugers Arch. 1993 Aug;424(3-4):266-75. doi: 10.1007/BF00384352.
Midbrain periaqueductal grey (PAG) provokes the defense reaction when stimulated. The present study was conducted to determine whether, and how, the PAG produces baroreflex inhibition, a feature characterizing the hypothalamic defense reaction. In chloralose-urethane anaesthetized rats, baroreflex vagal bradycardia and baroreflex hypotension were provoked by aortic depressor nerve stimulation. When the PAG was electrically stimulated baroreflex vagal bradycardia was remarkably suppressed; suppression of baroreflex hypotension was observed following bilateral vagotomy. In contrast, chemical stimulation of the PAG by D,L-homocysteic acid microinjection markedly suppressed baroreflex vagal bradycardia but only minimally suppressed baroreflex hypotension. These findings suggest that whereas overall PAG stimulation inhibits not only cardiac but also vascular components of baroreflexes, inhibition of the latter component either depends largely on activation of passing fibers or requires recruitment of a larger number of PAG cell bodies. PAG inhibition of baroreflex vagal bradycardia was not affected following spinal cord transection at C1, indicating that the inhibition was exclusively central in origin and not due to peripheral, prejunctional inhibition of vagal acetylcholine release by increased cardiac sympathetic nerve activities. The PAG inhibition of baroreflexes was greatly attenuated following electrolytic as well as chemical destruction of the parabrachial region. On the other hand, when the PAG was extensively lesioned, baroreflex inhibition produced by hypothalamic defense area stimulation was markedly diminished. PAG excitation thus causes powerful inhibition of arterial baroreflexes which is mediated by the parabrachial region; the PAG also mediates a major fraction of hypothalamic inhibition of the baroreflexes.
中脑导水管周围灰质（PAG）受到刺激时会引发防御反应。本研究旨在确定PAG是否以及如何产生压力反射抑制，这是下丘脑防御反应的一个特征。在氯醛糖-乌拉坦麻醉的大鼠中，通过刺激主动脉减压神经引发压力反射性迷走性心动过缓和压力反射性低血压。当电刺激PAG时，压力反射性迷走性心动过缓明显受到抑制；双侧迷走神经切断后观察到压力反射性低血压受到抑制。相比之下，通过微量注射D，L-高半胱氨酸对PAG进行化学刺激可明显抑制压力反射性迷走性心动过缓，但对压力反射性低血压的抑制作用很小。这些发现表明，虽然整体PAG刺激不仅抑制压力反射的心脏成分，也抑制血管成分，但后者的抑制要么很大程度上依赖于传入纤维的激活，要么需要募集更多的PAG细胞体。在C1水平进行脊髓横断后，PAG对压力反射性迷走性心动过缓的抑制作用不受影响，这表明该抑制完全起源于中枢，而非由于心脏交感神经活动增加对迷走神经乙酰胆碱释放的外周节前抑制。在臂旁区域进行电解以及化学破坏后，PAG对压力反射的抑制作用大大减弱。另一方面，当PAG广泛受损时，下丘脑防御区域刺激所产生的压力反射抑制明显减弱。因此，PAG兴奋会导致由臂旁区域介导的对动脉压力反射的强烈抑制；PAG还介导了下丘脑对压力反射抑制的大部分作用。
