[Effect of sympathectomy on responses of pial arteries during acute deficiency of cerebral blood supply]. / Vliianie simpatéktomii na reaktsii pial'nykh arterii pri ostrom defitsite krovosnabzheniia golovnogo mozga.

The dilatatory responses of small pial arteries including their active segments (sphincters at off-shoots, precortical arteries), to blood supply deficiency in the cerebral cortex were compared in control and sympathectomized rabbits. The sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls. The vasodilatation was much less obvious in sympathectomized than in control animals. This was associated with (and probably caused by) a considerable rise in histochemically detected serotonin activity of the pial arteries walls. After recovery of blood supply to the brain the constriction of the pial arterial active segments restricting the excessive cerebral blood flow, was significantly reduced due, probably, to the sympathetic deprivation. Therefore, the sympathetic control plays an important part in pial arterial responses regulating the adequate blood supply of the cerebral cortex.

[Histochemical studies of the microvascular effectors regulating blood supply to the cerebral cortex]. / Gistokhimicheskie issledovaniia mikrovaskuliarnykh éffektorov regulirovaniia krovosnabzheniia kory golovnogo mozga.

The innervation of the pial arteries as well as the activity of enzymes (phosphorylase I, II, III, succindehydrogenase, lactate dehydrogenase, ATPase, GTPase and CTPase) responsible for vascular smooth muscle function were studied histochemically on total microscopic preparations of rabbit pia matter. An especially rich adrenergic and cholinergic innervation was found around the active microvascular effectors - sphincters of pial and precortical arterial off-shoots. The nerve fibers followed the radial arteries entering the cerebral cortex. No differences were detected between the pial arteries and active microvascular effectors in the enzyme activity.