Abstract | INTRODUCTION: METHODS: SAH-induced vasospasm was modeled by contracting isolated segments of rat superior cerebellar arteries with a combination of serotonin and a synthetic analog of prostaglandin A(2). A pressure myograph system was used to determine vessel reactivity of spastic as well as non- spastic arteries. RESULTS: Compared to the initial vessel diameter, a combination of serotonin and prostaglandin induced considerable vasospasm (55 ± 2.5 % contraction; n = 12; p < 0.001). Locally applied nimodipine dilated the arteries in a concentration-dependent manner starting at concentrations as low as 1 nM (n = 12; p < 0.05). Concentrations higher than 100 nM did not relevantly increase the vasodilatory effect. Nimodipine's vasodilatory effect was smaller in spastic than in non- spastic vessels (n = 12; p < 0.05), which we assume to be due to structural changes in the vessel wall. CONCLUSION: The described ex vivo model allows to investigate the dose-dependent efficacy of spasmolytic drugs prior to in vivo experiments. Low concentrations of locally applied nimodipine have a strong vasodilatory effect, which is of relevance when considering the local application of nimodipine in cerebral vasospasm.
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Authors | Fatih Seker, Jürgen Hesser, Eva Neumaier-Probst, Christoph Groden, Marc A Brockmann, Rudolf Schubert, Carolin Brockmann |
Journal | Neuroradiology
(Neuroradiology)
Vol. 55
Issue 1
Pg. 71-6
(Jan 2013)
ISSN: 1432-1920 [Electronic] Germany |
PMID | 22864556
(Publication Type: Journal Article)
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Chemical References |
- Vasodilator Agents
- Nimodipine
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Topics |
- Animals
- Cerebral Arteries
(drug effects, physiopathology)
- Dose-Response Relationship, Drug
- Male
- Nimodipine
(administration & dosage)
- Rats
- Rats, Wistar
- Treatment Outcome
- Vascular Resistance
(drug effects)
- Vasodilator Agents
(administration & dosage)
- Vasospasm, Intracranial
(drug therapy, physiopathology)
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