Title

Dantrolene mediates vasorelaxation in cerebral vasoconstriction: a case series

UMMS Affiliation

Department of Neurology

Publication Date

8-13-2008

Document Type

Article

Subjects

Adult; Dantrolene; Female; Humans; Male; Middle Aged; Middle Cerebral Artery; Muscle Relaxants, Central; Regional Blood Flow; Subarachnoid Hemorrhage; Vasodilation; Vasospasm, Intracranial

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

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.

Rights and Permissions

Citation: Neurocrit Care. 2009;10(1):116-21. Epub 2008 Aug 12. Link to article on publisher's site

DOI of Published Version

10.1007/s12028-008-9133-4

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Neurocritical care

PubMed ID

18696267