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자료유형
학술저널
저자정보
저널정보
대한의생명과학회 대한의생명과학회지 대한의생명과학회지 제11권 제2호
발행연도
2005.6
수록면
211 - 219 (9page)

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Trigeminovascular system plays an important role for the cerebral hemodynamics. The aim of this study was to investigate the alterations in cerebrovascular reactivity by trigeminovascular system injury in rats. Trigeminovascular system of male Sprague-Dawley rats was injured by either denervation of nasocilliary nerve or neonatal capsaicin treatment. Trigeminovascular system was stimulated by controlled hemorrhagic hypotension or somatosensory (whisker) stimulation. Changes in regional cerebral blood flow (rCBF) and pial arterial diameter were continuously measured by laser-Doppler flowmetry and videomicroscopy, respectively. Nitric oxide synthase (NOS) activity in cerebral cortex was determined by measuring the conversion of L-<sup>3</sup>H-arginine to L-<sup>3</sup>H-citrulline. Cyclic GMP levels in cerebral cortex and pial artery were determined using the cyclic GMP <sup>125</sup>I scintillation proximity assay system. rCBF autoregulation was impaired or almost abolished by trigeminovascular system injury. rCBF response to whisker stimulation was significantly attenuated by trigeminovascular system injury. NOS activity as well as cyclic GMP level in cerebral cortex and pial artery were significantly reduced in the group of trigeminovascular system injury. These results suggest that trigeminovascular system injury causes prominent alterations in cerebrovascular reactivity, and that NO, which is generated by neuronal NOS in the trigeminovascular system is implicated in the regulation of rCBF.

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UCI(KEPA) : I410-ECN-0101-2009-510-017356472