Nakai M, Tamaki K, Ogata J, Maeda M
National Cardiovascular Center Research Institute, Osaka, Japan.
J Auton Nerv Syst. 1994 Sep;49 Suppl:S21-4. doi: 10.1016/0165-1838(94)90081-7.
We attempted to elucidate the vasomotor mechanisms regulating the cerebral circulation of rats under arterial hypertensive states of different origin. Sudden cold exposure elicited a cerebrovasodilator response mediated primarily by an enhanced cerebral metabolic state. The response was not modified by the concomitantly enhanced cerebrovascular sympathetic action. Central inhibition of the baroreceptor reflex, as achieved by chemical inhibition of the caudal ventrolateral medulla, disinhibited a non-metabolic cerebrovasodilator mechanism. However, its action was masked by a concomitantly enhanced sympathetic vasoconstrictor action. Another type of cerebrovasodilator response, also of non-metabolic origin, was elicited by chemical stimulation of the defence area within the periaqueductal grey matter. Thus, the cerebrovasomotor mechanisms are diversely activated so as to cope adequately with the individual conditions imposed on the animals.
我们试图阐明在不同起源的动脉高血压状态下调节大鼠脑循环的血管运动机制。突然的冷暴露引发了一种脑血管舒张反应,主要由增强的脑代谢状态介导。该反应并未因同时增强的脑血管交感神经作用而改变。通过化学抑制延髓尾端腹外侧来实现压力感受器反射的中枢抑制,解除了一种非代谢性脑血管舒张机制的抑制。然而,其作用被同时增强的交感神经血管收缩作用所掩盖。另一种同样是非代谢起源的脑血管舒张反应是由化学刺激导水管周围灰质内的防御区域引起的。因此,脑血管运动机制被多种方式激活,以便充分应对施加于动物的个体状况。