Abstract
In the earlier communication of the experimental subarachnoid hemorrhage (SAH), one of the authors (Tanaka) reported that the administration of fusaric acid, a potent inhibitor of dopamine-β-hydroxylase, completely relieved the vasospasm in the acute phase of the disease, and that the noradrenergic system seemed to participate in the pathogenesis of the vasospasm. The present study was designed to know whether the same mechanism is operating on the vasospasm in the chronic phase of SAH.
Twenty cats of either sex, weighing 1.8 to 3.5 Kg, were used, and the experimental SAH was produced by the cisternal injection of fresh autogenous blood. The effect of intravenous injection of fusaric acid (50 mg/kg) on the diameter of pial arteries was evaluated either 3 days (Experiment 1) or 7 days (Experiment 2) after SAH by means of the microphotographic technique through a cranial window. The cerebral blood flow was also measured by the hydrogen clearance method.
The results of the experiments were as follows;
Experiment 1 : The pial arteries were dilated significantly (p<0.005-0.01) after the administration of fusaric acid. The degree of the dilatatory response was greater than that in the control group.
Experiment 2 : The vasospasm, which appeared immediately after SAH, showed a spontaneous gradual relief on the first day, but it recurred 4 days later and continued to show an aggravation until the 7th day when fusaric acid was administered. Immediately after the injection of the agent the vasospasm started to ameliolate and disappeared completely 90 minutes later. Fusaric acid also remarkably improved the cerebral blood flow in spite of the reduction of arterial blood pressure.
The above data suggest that the noradrenergic system participates in the vasospasm of the chronic phase of SAH.
