Sadoshima S, Busija D W, Heistad D D
Am J Physiol. 1983 Mar;244(3):H406-12. doi: 10.1152/ajpheart.1983.244.3.H406.
The purpose of this study was to examine mechanisms by which sympathetic nerves protect against cerebral hemorrhage and ischemic infarction (i.e., "stroke") in stroke-prone spontaneously hypertensive rats (SHRSP). When unilateral superior cervical ganglionectomy was performed in SHRSP at 1 mo of age, development of cerebral vascular hypertrophy was inhibited and stroke developed only in the denervated hemisphere in 79% of the rats (P less than 0.05). Because "trophic" effects of sympathetic nerves on vascular growth may be less in older animals, unilateral sympathetic denervation was performed in SHRSP at 3 mo of age. The incidence of stroke was similar in the innervated and denervated hemispheres. In another group of rats that had unilateral ganglionectomy at 1 mo, we examined regulation of cerebral blood flow (CBF) when the rats were 4-5 mo of age, before neurologic signs of stroke. CBF, measured with microspheres, was similar in the innervated and denervated hemispheres during control conditions and during maximal vasodilatation produced by bicuculline. In contrast, when mean arterial pressure was raised acutely, CBF increased more in the denervated hemisphere than in the innervated hemisphere. We conclude that 1) in contrast to effects of denervation at 1 mo, sympathetic denervation at 3 mo of age (when trophic effects are less) does not lead to stroke, and 2) chronic denervation impairs the cerebral vasoconstrictor response to acute increases in arterial pressure.
本研究的目的是探讨交感神经在易患中风的自发性高血压大鼠(SHRSP)中预防脑出血和缺血性梗死(即“中风”)的机制。当在1月龄的SHRSP中进行单侧颈上神经节切除时,脑血管肥大的发展受到抑制,79%的大鼠仅在去神经支配的半球发生中风(P<0.05)。由于交感神经对血管生长的“营养”作用在老年动物中可能较小,因此在3月龄的SHRSP中进行单侧交感神经去神经支配。去神经支配半球和未去神经支配半球的中风发生率相似。在另一组1月龄时进行单侧神经节切除的大鼠中,我们在大鼠4-5月龄、出现中风神经症状之前,检测了脑血流量(CBF)的调节情况。在对照条件下以及在荷包牡丹碱产生的最大血管舒张期间,用微球测量的CBF在去神经支配半球和未去神经支配半球中相似。相反,当平均动脉压急性升高时,则去神经支配半球的CBF增加幅度大于未去神经支配半球。我们得出结论:1)与1月龄时去神经支配的作用相反,3月龄时(营养作用较小)交感神经去神经支配不会导致中风;2)慢性去神经支配会损害大脑对动脉压急性升高的血管收缩反应。