Abstract
The effect of sympathetic stimulation on resting cerebral blood flow (CBF) is still somewhat controversial, although the adrenergic innervation of both pial and intraparenchymal arteries was confirmed histochemically. Harper assumed that the neurogenic constriction of extraparenchymal vessels might be countervailed by the metabolic dilation of intraparenchymal vessels.
To test his hypothesis, the responses of both pial and intraparenchymal vessels to the sympathetic stimulation were investigated in 9 cats by means of a new method. This method consists of the videocamera system already established and the photoelectric system to estimate local cerebral blood volume (CBV). Two cranial windows were placed in the unilateral parietal skull of the cats at the distance of 3 mm. The brain surface under one cranial window was lighted by an optical fiber derived from a halogen lamp. The same illumination was utilized for simultaneous measurements of both pial vessel diameters and CBV. A silicon photodiode was attached to another window to measure the intensity of scattering light through the brain tissue, which mainly reflected changes in blood volume of the intraparenchymal vessels (arteriolescapillariesvenules). This method permits atraumatic simultaneous analysis of both superficial and deep cerebral circulation. The ipsilateral superior cervical ganglion was stimulated electrically (3-8V, 300μsec, 100Hz) for 5 minutes.
Initially, both pial and intraparenchymal vessels constricted and reached their maximum constriction at 79±14 seconds in intraparenchymal vessels, at 130±30 seconds in pial veins and at 179±37 seconds in pial arteries. The maximum constriction of intraparenchymal vessels occured earlier than that of pial arteries (p<0.05). The maximum constriction rates of pial arteries and veins were 10.7±3.0% and 6.3±2.3% respectively without significant statistical difference. The pial arteries remained constricted throughout the stimulation, however, the intraparenchymal vessels started to dilate at 79±14 seconds. The dilation continued to exceed the control level at 238±39 seconds even during the stimulation.
In conclusion, the sympathetic vasoconstriction occured in both pial and intraparenchymal vessels. The compensatory metabolic dilation of intraparenchymal vessels was delayed 4 minutes after the initiation of the stimulation.
