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Elevated transferrin concentration in cerebral spinal fluid after subarachnoid hemorrhage
K V Takenaka1, N Sakai, S Murase
1Department of Neurosurgery, Gifu University School of Medicine, Gifu, Japan. kat927@oregano.ocn.ne.jp
Neurological Research
|January 10, 2001
Summary
Transferrin (TF) levels in cerebrospinal fluid (CSF) are elevated after subarachnoid hemorrhage (SAH). This elevation correlates with cerebral vasospasm and may contribute to its development by inducing nitric oxide synthase.
Area of Science:
- Neuroscience
- Biochemistry
- Pathophysiology
Background:
- Subarachnoid hemorrhage (SAH) is a critical condition often leading to cerebral vasospasm.
- The exact molecular mechanisms underlying SAH-induced vasospasm remain incompletely understood.
- Transferrin (TF), a key iron-binding protein, has been implicated in various physiological and pathological processes.
Purpose of the Study:
- To investigate the concentration of Transferrin (TF) in cerebrospinal fluid (CSF) following subarachnoid hemorrhage (SAH).
- To evaluate the effects of TF on cultured smooth muscle cells (SMCs) to understand its role in cerebral vasospasm.
- To explore the potential link between TF, nitric oxide production, and vasospasm development after SAH.
Main Methods:
- Cerebrospinal fluid (CSF) samples were collected from SAH patients and control subjects.
- TF concentrations in CSF were measured using the Speriol micro-transferrin assay.
- Effects of TF on cultured SMCs were assessed by measuring nitrite accumulation and inducible nitric oxide synthase (iNOS) mRNA levels.
Main Results:
- TF was undetectable in control CSF but quantifiable in all SAH patients.
- Significantly higher TF levels were observed in SAH patients with vasospasm compared to those without.
- TF exposure in vitro increased nitrite accumulation and induced iNOS mRNA expression in SMCs.
Conclusions:
- Elevated TF concentrations in CSF after SAH are associated with cerebral vasospasm.
- TF may contribute to vasospasm development by inducing iNOS in vascular smooth muscle cells.
- TF represents a potential biomarker and therapeutic target in managing SAH complications.