Dantrolene mediates vasorelaxation in cerebral vasoconstriction: a case series
UMass Chan Affiliations
Department of NeurologyDocument Type
Journal ArticlePublication Date
2008-08-13Keywords
AdultDantrolene
Female
Humans
Male
Middle Aged
Middle Cerebral Artery
Muscle Relaxants, Central
Regional Blood Flow
Subarachnoid Hemorrhage
Vasodilation
Vasospasm, Intracranial
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
INTRODUCTION: Cerebral vasoconstriction syndromes such as vasospasm after subarachnoid hemorrhage (SAH) and trauma, or Call-Fleming syndrome are difficult to treat, and can lead to substantial disability and death. Dantrolene, a ryanodine receptor antagonist, inhibits intracellular calcium release from the sarco-endoplasmic reticulum. We examined the effect of dantrolene on middle cerebral artery (MCA) blood flow velocities as measured by transcranial Doppler (TCD). METHODS: Three consecutive patients with elevated MCA TCD velocities receiving dantrolene (2.5 mg/kg i.v. q6h) were retrospectively reviewed. Average MCA peak systolic, mean flow velocities, and the pulsatility index (PI) before and after the dantrolene infusion were compared within patients. Systemic physiological parameters (blood pressure, heart rate, central venous pressure, intracranial pressure, body temperature, and cooling water temperature) were retrospectively collected 6 h before and after the dantrolene infusion. RESULTS: MCA peak systolic velocities (mean +/- SE) for the three patients were 297 +/- 3, 248 +/- 8, and 268 +/- 19 cm/s before dantrolene and 159 +/- 9, 169 +/- 8, and 216 +/- 12 cm/s after dantrolene. Average mean flow velocities showed the same trend. Interestingly, the PI increased slightly from 0.6, 0.52, and 0.67 before dantrolene, to 1.17, 0.71, and 0.77 after dantrolene. Systemic physiological parameters remained stable in all three patients. CONCLUSION: Dantrolene attenuated cerebral vasoconstriction as measured by TCD without altering systemic physiological parameters. This suggests that intracellular calcium release from ryanodine channels in smooth muscle might play a role in vasospasm. A prospective study is underway to test this hypothesis.Source
Neurocrit Care. 2009;10(1):116-21. Epub 2008 Aug 12. Link to article on publisher's site
DOI
10.1007/s12028-008-9133-4Permanent Link to this Item
http://hdl.handle.net/20.500.14038/39187PubMed ID
18696267Related Resources
ae974a485f413a2113503eed53cd6c53
10.1007/s12028-008-9133-4