A new approach to the treatment of cerebral vasospasm: the angiographic effects of tadalafil on experimental vasospasm.
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.


CONCLUSIONS
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.
Koktekir
Ender
E
Neurosurgery Department, Ministry of Health Ankara Education and Research Hospital, Ankara, Turkey. enderkoktekirnrs@hotmail.com
Erdem
Yavuz
Y
Akif Bayar
Mehmet
M
Gokcek
Cevdet
C
Karatay
Mete
M
Kilic
Celal
C
D000818:Animals; D001488:Basilar Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D002243:Carbolines / Q000494:pharmacology* / Q000627:therapeutic use; D002533:Cerebral Angiography; D002536:Cerebral Arteries / Q000000981:diagnostic imaging* / Q000187:drug effects* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D006152:Cyclic GMP / Q000819:agonists / Q000378:metabolism; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D008297:Male; D009569:Nitric Oxide / Q000819:agonists / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D000068581:Tadalafil; D013997:Time Factors; D016896:Treatment Outcome; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use; D020301:Vasospasm, Intracranial / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000503:physiopathology
D002243:Carbolines; D010726:Phosphodiesterase Inhibitors; D014665:Vasodilator Agents; D009569:Nitric Oxide; D000068581:Tadalafil; D006152:Cyclic GMP