A new approach to the treatment of cerebral vasospasm: the angiographic effects of tadalafil on experimental vasospasm
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- Koktekir, E., Erdem, Y., Akif Bayar, M. et al. Acta Neurochir (2010) 152: 463. doi:10.1007/s00701-009-0540-x
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.
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.
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.
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.
KeywordsCerebral vasospasm Nitric oxide Tadalafil Angiography
cyclic guanosine monophosphate
delayed ischemic neurological deficit
endothelium-derived constrictor factor
endothelium-derived releasing factor
endothelial nitric oxide synthase