Dantrolene Mediates Vasorelaxation in Cerebral Vasoconstriction: A Case Series
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ORIGINAL ARTICLE
Dantrolene Mediates Vasorelaxation in Cerebral Vasoconstriction: A Case Series Susanne Muehlschlegel Æ Guy Rordorf Æ Michael Bodock Æ John R. Sims
Published online: 12 August 2008 Ó Humana Press Inc. 2008
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, Dr. John Sims is supported by NIH 1 K08 NS049241-01A2. None of the authors have any conflict of interest. S. Muehlschlegel Departments of Neurology, Anesthesiology/Critical Care and Surgery, UMASS Memorial Medical Center, University Campus, University of Massachusetts Medical School, Worcester, MA, USA G. Rordorf J. R. Sims Department of Neurology, Neurocritical Care and Acute Stroke, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA M. Bodock Department of Pharmacy, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA J. R. Sims (&) Department of Radiology, Massachusetts General Hospital, Harvard Medical School, CNY149 Rm 6212A, Charlestown, MA 02129, USA e-mail: [email protected]
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. Keywords Subarachnoid hemorrhage Vasospasm Cerebral vasoconstriction Dantrolene Transcranial Doppler Delayed ischemic neurologic deficit
Background Cerebral vasoconstriction syndromes are frequently observed in the neuroscience intensive care unit (neuroICU) and can cause ischemia. They include Call–Fleming syndrome [1] and cerebral vasos
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