Background: The pathogenesis of cerebral vasospasm is likely to be multifactorial. Strong evidence has indicated that decreasing levels of NO after SAH seem to be important. A PDE-V inhibitor, tadalafil, theoretically increases NO levels. Our study investigated the vasodilatory efficacy of tadalafil on the cerebral arteries with measurement of basilar artery diameters on angiography.
Methods: We used 42 male Wistar-Albino rats to test our hypothesis. They were assigned randomly into the following seven groups: group 1: control (only saline), group 2: SAH only (killed on day 2), group 3: SAH + tadalafil (killed on day 2), group 4: SAH only (killed on day 4), group 5: SAH + tadalafil (killed on day 4), group 6: saline + tadalafil (killed on day 2) and group 7: saline + tadalafil (killed on day 4). The three different parts of basilar artery diameters were measured angiographically.
Results: There were statistically significant differences between the SAH and SAH groups treated with tadalafil at days 2 and 4. Comparison between control and tadalafil groups showed no significant differences. This result indicated that tadalafil has a vasodilatory effect on vasoconstricted arteries, but no effect on normal basilar arteries.
Conclusion: Our study results showed that tadalafil has a vasodilatory effect on both acute and chronic periods of cerebral vasospasm. We also concluded that cerebral angiography can be used safely for investigation of cerebral vasospasm in animal studies.
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