Abstract
α2-adrenoceptor has been shown to exist in the noradrenergic nerve terminals and smooth muscles of the cerebral arteries, and also in the brainstem. In order to investigate the role of α2-adrenoceptor in cerebral hemodynamics, the effects of clonidine, a potent α2-agonist, on the diameter and autoregulatory response of feline pial arteries were observed.
Thirteen adult cats were anesthetized with intraperitoneal injection of α-chloralose (50 mg/kg) plus urethane (500 mg/kg), and ventilated with a respirator. The diameter of the pial arteries was measured continuously through a cranial window by means of a video camera system developed in our laboratory.
Intravenous injection of clonidine (100 μg/kg) produced an initial transient increase in arterial blood pressure followed by a gradual decrease. However, intracarotid administration of clonidine (10 μg/kg) reduced the blood pressure from the beginning but less markedly.
Clonidine injected either intravenously or intracarotidly produced a transient constriction of the pial arteries followed by a gradual dilatation, which was more marked in the latter group.
The effects of clonidine on the autoregulatory response of the pial arteries were observed during hemorrhage and reinfusion of the blood. After intravenous administration of clonidine, the vasoconstrictive response of the pial arteries during reinfusion of the blood was significantly disturbed compared with the vasodilatory response during hemorrhage of the blood. After intracarotid injection of clonidine, where the amount of the agent reached the brainstem was assumed to be relatively small, there was no marked change either in the vasodilatory or in the vasoconstrictive response of the pial arteries.
The above data suggest the importance of α2-adrenoceptor both in regulation of pial arterial diameter and in autoregulation of cerebral blood flow.
