Elevated transferrin concentration in cerebral spinal fluid after subarachnoid hemorrhage.

Calcium-elevating protein cross-reacted with anti-human transferrin (TF) was purified in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). The concentration of TF in CSF after SAH was measured, and the effects of TF on cultured smooth muscle cells (SMCs) were evaluated in order to understand the relationship between TF and cerebral vasospasm. Cisternal CSF samples were collected from 12 patients (seven men and 13 women) with SAH due to the rupture of a cerebral aneurysm, and eight control subjects. The patients were divided into two groups: (1) those presenting no clinical and radiological evidence of vasospasm (the non-vasospasm group; three men and 10 women, mean age 54.7 years), and (2) those presenting evidence of vasospasm (the vasospasm group; four men and three women, mean age 58.3 years). The concentration of TF in CSF was measured using Speriol micro-transferrin measure assay method. Nitrite accumulation in the culture media of SMCs incubated with TF was determined by diazotization method. The mRNA levels of inducible isoform of NOS (iNOS) in SMC incubated with TF were measured by the reverse transcription-coupled polymerase chain reaction method. Levels of TF were markedly different in the SAH and the control subjects. In the control group, all subjects had no detectable quantity of TF. In contrast, all patients after SAH had quantifiable TF in their CSF. Moreover, there was a significant difference between the vasospasm group and the non-vasospasm group in TF levels (p < 0.05). In the vasospasm group, the average value was 10.43 +/- 2.8 mg dl-1. In the non-vasospasm group, the average was 3.69 +/- 0.31 mg dl-1. The nitrite content in the culture medium incubated with TF was three times the content of control. TF also induced iNOS mRNA in SMC. This study demonstrated that an elevation of TF concentration in CSF after SAH was detected and iNOS mRNA in SMCs was also induced by TF. This may be involved in some roles of the development of the pathological series of events after SAH, including vasospasm.