Nakai M, Maeda M
National Cardiovascular Center Research Institute, Osaka, Japan.
Neuroscience. 1994 Feb;58(4):785-91. doi: 10.1016/0306-4522(94)90455-3.
We attempted to elucidate the mechanisms operating in the mediation of the cerebrovasodilator action of the defence area within the periaqueductal gray matter, employing radiolabelled microsphere flowmetry in 50 anaesthetized rats. The caudal two-thirds of this brain region were chemically stimulated with N-methyl-D-aspartate (1 nmol as 100 nl in a 10-mM solution). Besides eliciting a distinctive pattern of haemodynamic defence responses, the stimulation consistently provoked a cerebrovasodilator action, preferentially in the supratentorial brain regions. In particular, 56% of the overall flow increase in the parasagittal cerebral cortex was solely attributable to the unique cerebrocortical vasodilator action of the periaqueductal gray matter, independent of unspecific effects of concomitantly occurring hypertension itself. This flow change was not associated with a specific change in the metabolic rate for O2 of this cortical region. We conclude that the major part of the unique cerebrocortical vasodilator action provoked from the defence area within the periaqueductal gray matter was mediated by non-metabolic mechanisms. The involvement of the metabolic mechanism could be of only minor importance, if any. Cerebral vasodilatation may be involved in the natural defence reactions for coping with the emergency that threatens the animal.
我们试图阐明中脑导水管周围灰质内防御区域介导脑血管舒张作用的机制,在50只麻醉大鼠中采用放射性微球血流测定法。用N-甲基-D-天冬氨酸(1纳摩尔,以100纳升的量溶于10毫摩尔的溶液中)对该脑区尾侧三分之二进行化学刺激。除了引发独特的血流动力学防御反应模式外,这种刺激还持续引发脑血管舒张作用,优先作用于幕上脑区。特别是,矢状旁大脑皮质总体血流增加的56%完全归因于中脑导水管周围灰质独特的脑血管皮质舒张作用,与同时发生的高血压本身的非特异性效应无关。这种血流变化与该皮质区域的氧代谢率的特定变化无关。我们得出结论,中脑导水管周围灰质内防御区域引发的独特脑血管皮质舒张作用的主要部分是由非代谢机制介导的。代谢机制的参与即使有也可能只起次要作用。脑血管舒张可能参与了应对威胁动物的紧急情况的自然防御反应。