抄録
Intracranial blood vessels are apparently innervated by catecholaminergic neuron. Until now, little is known about the function of these nerve plexes. Some scattered evidence suggests that these perivascular nerve has regulatory function toward cerebral circulation.
To find out its role, experimental cerebral ischemia was produced by temporary occlusion of middle cerebral artery (MCA) in rhesus monkey. Transorbital microsurgical technique was employed for exposing the origin of MCA. Cerebral blood flow was assessed by measurement of the cortical temperature (Tc), using thermister placed on anterior temporal lobe. Following the application of small Scoville clip to MCA, Tc on the same side fell down to certain degree (mean fall of Tc = -2.9 ± 0.6°C) and restoration of flow raised Tc to approximately the same degree (mean rise of Tc = +3.1 ± 0.7°C). Pressure autoregulation (PAR) of cerebral blood flow was examined following the elevation of mean arterial blood pressure by inflation of the aortic balloon.
Three hours occlusion of MCA did not harm PAR, but it became disturbed after five hours in control animals. Following presumptive chemical sympathectomy produced by administration of either L-alpha-methyl-tyrosine or 3-alpha-dimethyl-tyrosine, PAR appeared to be lost on the side of the occlusion alone when MCA occlusion lasted 1.5 hours or longer. Reactivity to hypercapnia and hypocapnia was preserved on both control and chemical sympathectomy groups even after MCA occlusion.
Based on these observations, it was suggested that sympathetic control of cerebral circulation was necessary for counteracting the postischemic vasodilatation with maintaining the proper pressure autoregulation.
