Summary: CBF, as measured by the clearance of 133Xe or 85Kr in the pentobarbital-anesthetized cat, displays a monotonic increase as the Pac02 is elevated over a range of 20-60 mm Hg (slope Xe, 1.65 ± 0.14 mill 00 glminlmm Hg; slope Kr, 1.40 ± 0.11 mlllOO glminlmm Hg). Cloni dine (20 fLg/kg i.v.), a centrally acting, cx2-preferring ago nist, reduced the slope of the Pac02-CBF response func tions for Xe and Kr by 70 and 64%, respectively. Cloni dine reduced normocarbic CBF -Xe by 36%, but had no effect on normocarbic CBF-Kr. ST-91, a polar structural analog of clonidine that does not cross the blood -brain barrier, did not reproduce the effects of clonidine when administered at an equivalent dose. This indicates that the effects of clonidine observed were secondary to its action on central rather than peripheral sites. In additionThe role of intrinsic neural systems in the regula tion of cerebral circulation has been a subject of controversy over the last decade. Several lines of evidence exist to indicate the possible role of a cen tral adrenergic substrate.First, fluorescence histochemical studies have indicated the existence of rich perivascular nor adrenergic innervation. The innervation of the major cerebral arteries, their pial branches, and to a lesser degree penetrating arterioles as small as 15 fLm in diameter, arise from the ipsilateral superior cervical ganglion (Edvinsson et aI. , 1973). The in trinsic system of cerebrovascular innervation in volving noradrenergic neurons, however, arises largely from the locus ceruleus, with widespread axonal projections that appear to terminate on small intraparenchymal vessels (Rennels and Nelson, 1975).Second, microapplication-superfusion studies of pial vessels in vivo and ex vivo have demonstrated
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