Abstract
The pathophysiology of cerebral arterial spasms after subarachnoid hemorrhage (SAH) are not well known yet. This study was designed to clarify the role of noradrenergic system in the spasm.
Effects of fusaric acid (F.A.), a potent inhibitor of dopamine-β-hydroxylase, on pial arterial diameter and regional cerebral blood flow (r-CBF) were investigated in 16 cats with pial arterial spasm after experimental SAH. Cats were anesthetized with α-chloralose (50 mg/kg) and urethane (500 mg/kg). After the administration of alcuronium chloride, respiration was maintained constant throughout the experiment. Parietal craniectomy was performed for the microphotographic observation of pial vessels. r-CBF were measured by the hydrogen clearance method in four regions of the brain. Vasospasms were induced by the cisternal injection of the fresh autogenous blood (group 1 (8 cats)) or the mixture of autogenous blood and CSF incubated for 4 days (group 2 (8 cats)). F.A. (50 mg/kg) was administered intravenously 45 to 50 minutes after the cisternal injection.
The following results were obtained.
1) In both groups, the diameters of pial arteries began to decrease significantly (p<0.001-0.005) immediately after the cisternal injection. These arterial spasms continued up to the time of administration of F.A. r-CBF showed. a reduction almost in parallel with the decrease of pial arterial diameters in all regions. The degree of vasospasm and r-CBF reduction in group 2 were more marked than those in group 1.
2) Intravenous injection of F.A. resulted in a complete disappearance of the spasm (p<0.001) and the r-CBF rapidly restored and even exceeded the control level in spite of a moderate fall of blood pressure. In either group maximum effects of the drug were observed 40 minutes after the administration of the agent.
The above data suggest the participation of the activity of noradrenergic nerve endings in the pathogenesis of cerebral arterial spasm after SAH.
