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Background: In medically refractory vasospasm, invasive intervention may be required. A commonly used approach is intra-arterial (IA) drug infusion. Although calcium channel blockers (CCBs) have been widely applied in this setting, studies comparing their efficacies and durations of action have been few. This study was performed to compare attributes of three CCBs (nicardipine, nimodipine, and verapamil), focusing on duration of the vasodilatory action based on angiography. Methods: Vasospasm was produced in New Zealand white rabbits (N = 22) through experimentally induced subarachnoid hemorrhage and confirmed in each via conventional angiography, grouping them by IA-infused drug. After chemoangioplasty, angiography was performed hourly for 5 h to compare dilated and vasospastic arterial diameters. Drug efficacy, duration of action, and changes in mean arterial pressure (relative to baseline) were analyzed by group. Results: Effective vasodilation was evident in all three groups immediately after IA drug infusion. The vasodilative effects of nimodipine and nicardipine peaked at 1 h and were sustained at 2 h, returning to initial vasospastic states at 3 h. In verapamil recipients, effects were more transient by comparison, entirely dissipating at 1 h. Only the nicardipine group showed a significant 3-h period of lowered blood pressure. Conclusions: Although nimodipine and nicardipine proved longer acting than verapamil in terms of vasodilation, their effects were not sustained beyond 2 h after IA infusion. Further study is required to confirm the vasodilatory duration of IA CCB based on perfusion status, and an effort should be made to find new alternative to extend the duration. [ABSTRACT FROM AUTHOR]

Vigabatrin, an antiepileptic drug, increases the level of gamma aminobutyric acid in the brain by inhibiting its catabolism. Because gamma aminobutyric acid has been proved to have vasodilatory effects, in the present study, we investigated the effect of vigabatrin to treat experimental subarachnoid hemorrhage (SAH)-induced vasospasm. A total of 30 New Zealand white rabbits were divided into 3 groups of 10 each: the control group, SAH group, and vigabatrin group. Experimental SAH was established by injection of autologous arterial blood into the cisterna magna. In the vigabatrin group, the rabbits were administered vigabatrin for 3 days after induction of the SAH. The first dose of vigabatrin was given 2 hours after SAH induction. A daily dose of 500 mg/kg vigabatrin was administered intraperitoneally. After 3 days, the rabbits were sacrificed, and the brains were removed, together with the cerebellum and brainstem. The basilar artery wall thickness and lumen areas were measured. The neuronal degeneration in the hippocampus (CA1, CA3, and dentate gyrus) was also evaluated. The arterial wall thickness of the vigabatrin group was less than that in the SAH group (P < 0.001), and the mean luminal area of the vigabatrin group was greater than that in the SAH group (P < 0.001). Additionally, the hippocampal neuronal degeneration score of the vigabatrin group was lower than that of the SAH group (P < 0.001). These findings have indicated that vigabatrin has a vasodilatory effect in an experimental SAH model in the rabbit. Moreover, it showed a neuroprotective effect in the hippocampal neurons against secondary injury induced by SAH. [ABSTRACT FROM AUTHOR]

The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The cross-sectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment. [ABSTRACT FROM AUTHOR]