Objective: intrathecal administration of calcium channel antagonists has been proposed to reduce cerebral vasospasm (CVS) in animal subarachnoid hemorrhage (SAH) models. Also, delayed CVS treatment model with oral administration of cilostazol can be seen in the literature.
Methods: in this study, 25 male New Zealand white rabbits were randomly assigned to five groups: control, SAH only, SAH/nimodipine, SAH/cilostazol, SAH/vehicle. The animals' basilar arteries were sectioned from four separate zones and four sections were obtained from each rabbit. Basilar artery luminal section areas were measured by using SPOT for windows Version 4.1 computer program.
Results: basilar artery luminal section areas in SAH/ nimodipine and SAH/ cilostazol groups were significantly higher than SAH only group (P < 0.05).
Conclusion: phosphodiesterase 3 inhibitor cilostazol has vasodilatory effects without affecting cerebral blood flow. Nimodipine is a calcium channel blocker and is still used in vasospasm therapy either oral or intravenously. This study demonstrates that prophylactic bolus intrathecal administration of either cilostazol or nimodipine equally prevents SAH-associated CVS in an animal model. We therefore propose that cilostazol is a candidate for clinical trials in the treatment of delayed vasospasm.