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JOURNAL OF NEUROSURGICAL SCIENCES
Rivista di Neurochirurgia
Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651
Journal of Neurosurgical Sciences 2012 December;56(4):363-71
Dexamethasone significantly attenuates sub-arachnoid hemorrhage-induced elevation in cerebrospinal fluid citrulline and leukocytes
Spratt D. E. 1, Reddy V. K. 2, Choxi A. A. 2, Simon S. D. 3, Shay S. D. 2, Davidson M. A. 4, Barr F. E. 5, Summar M. L. 6, Mericle R. A. 7 ✉
1 Department of Radiation Oncology, Memorial-Sloan Kettering, New York, NY, USA;
2 Department of Neurological Surgery, Vanderbilt University Medical Center, Nashville, TN, USA;
3 Department of Neurological Surgery, Virginia Commonwealth University Medical Center Richmond, VI, USA;
4 Department of Biostatistics, Vanderbilt , University Medical Center, Nashville, TN, USA;
5 Pediatric Critical Care and Clinical and Translational Research Center, Cincinnati Children’s Hospital and Medical Center, Cincinnati, OH, USA;
6 Division of Genetics and , Metabolism Children’s National Medical Center Washington, DC, USA;
7 HW Neurological Institute, Nashville, TN, USA
AIM: Cerebral vasospasm is a leading cause of death and disability following aneurysmal subarachnoid hemorrhage (SAH). Nitric oxide (NO) is a potent mediator of vasodilation, and citrulline is a known contributor to NO production. The leukocytosis inflammatory response can increase vasoconstrictive compounds that may also contribute to vasospasm. Dexamethasone is a glucocorticosteroid commonly administered after SAH, which may alter the production of leukocytes and citrulline. The goal of this project was to study the effects of dexamethasone on leukocytosis, citrulline, and angiographic vasospasm.
METHODS: Experimental SAH was induced in 18 New Zealand white rabbits. Intravenous dexamethasone was administered to one group (N.=9) at 2 mg/kg/day. A placebo group (N.=9) was given a saline infusion with otherwise identical procedures. CSF citrulline, leukocytes, protein, and glucose, as well as plasma citrulline were measured at baseline and 3 days post-SAH in a blinded fashion. Basilar artery angiography was performed at baseline and repeated 3 days post-SAH.
RESULTS: The change in CSF citrulline from day 0 to day 3 was significantly lower in the dexamethasone group compared to controls (P=0.002). The change in CSF white blood cells was also significantly lower (P=0.005). There was no significant change in plasma citrulline levels or angiographic vasospasm.
CONCLUSION: Dexamethasone significantly decreases CSF citrulline and CSF leukocytosis after experimental SAH. It is possible this could lead to a relative vasoconstriction and vasodilation, respectively. These processes could cancel-out opposing effects of dexamethasone on cerebral vasospasm, partially contributing to the recognized, multifactorial, inconsistent effects of glucocorticoids on vasospasm.