Presentation
# 7
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6th Internet World Congress for Biomedical Sciences |
Satoshi Iwabuchi(1), Yasushi Sakai(2), Hitoshi Kimura(3), Shinya Yoshii(4), Tetsuya Yokouchi(5), Morikazu Ueda(6), Hirotsugu Samejima(7)
(1)(3)(4)(5)(6)(7)Department of Neurosurgery. Toho University - Tokyo. Japan
(2)Department of Physiology. Showa University College of Medical Sciences - Japan
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Bloody CSF collected from patients with SAH has been reported to produce sustained contractions of canine cerebral arteries (15) and human cerebral arteries (16,17,18,19). Takenaka, et al., (20) reported that CSF from patients with SAH induced cytosolic free Ca2+ elevations in single smooth-muscle cells which were prepared from explants of rat thoracic aorta. In the present study, CSF from all patients with aneurysmal SAH induced contraction of cerebrovascular smooth-muscle cells freshly isolated from rat basilar artery, and an increase of intracellular free Ca2+ concentration ([Ca2+]i) correlated with the contraction induced by CSF. Previously we showed that erythrocyte lysate produced [Ca2+]i elevation in cerebral smooth-muscle cells, and that tyrosine phosphorylation might be involved in erythrocyte lysate-induced [Ca2+]i elevation (14). The results of the present study suggest that some spasmogenic compound, possibly erythrocyte component or its breakdown products, is released into CSF after SAH. The contraction may involve an increase of [Ca2+]i that may be mediated by the activation of tyrosine kinase, protein kinase C and/or other kinases. In this study, CSF obtained on Day 3 following SAH induced greater contraction than that induced by CSF obtained on Day 7. There was a discrepancy between this observation and the fact that the peak of clinical vasospasm occurs about 7 days after SAH. Therefore, some spasmogens released into CSF after SAH may take a few days to affect smooth-muscle cells in the media via the adventitia. Takenaka, et al., (20) demonstrated that the changes in [Ca2+]i plotted over time after SAH in a vasospasm patient group (clinical and radiological evidence of vasospasm) showed a biphasic pattern, with the highest concentrations on Day 2 and 11, and that on Day 2, the [Ca2+]i elevation induced by CSF in the vasospasm group was significantly higher than that in the non-vasospasm group. In our study, there was no difference between the contraction caused by CSF from patients with clinical or radiological vasospasm, and that caused by CSF from patients without clinical or radiological vasospasm. There was no significant difference in the contractions caused by application of CSF after heating and by application of untreated CSF. These results indicate that some substances other than proteins or peptides are related to vasospasm following SAH. Preincubation of cells with suramin, an antagonist of P2x and P2y purinoceptors, attenuated contraction caused by application of CSF. Purine nucleotides may be involved in the contraction of cerebrovascular smooth-muscle cells after SAH. We are presently determining the level of adenine nucleotides such as ATP, ADP, AMP, adenosine and adenine in CSF samples, by high-performance liquid chromatography (HPLC) analysis.
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