• Herbal Formula Science
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• v.6 no.1
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• pp.187-197
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• 1998

The study was aimed to investigate the effect cuscutae semen(CS) on the vascular systems including changes in blood pressure (BP), regional cerebral blood flow(rCBF) and pial arteriolar diameter of male Sprague-Dawely rats. The changes in rCBF were determinated by laser-Doppler flowmetry, and the changes in diameter of pial arteriole were measured through a closed crainal window. 1. Blood pressure was not affected by CS in rats. 2. rCBF was increased by CS in a dose-dependent manner. 3. Pretreatment with methylene blue(Img/kg), and propranolol(1mg/kg) significantly inhibited CS induced increased in rCBF. 4. Pretreatment with indomethacin(1mg/kg) did not inhibited CS induced increased in rCBF. 5. Pial arterial diameter was increased by CS in a dose-dependent manner. These results suggest that CS causes a diverse response of blood pressure, regional cerebral blood flow(rCBF), and pial arteral diameter. The increased in rCBF is also mediated by adrenergic ${\beta}-receptor $ and guanylate cyclase.

• The Korean Journal of Pharmacology
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• v.29 no.1
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• pp.1-8
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• 1993

To elucidate involvement of platelet-activating factor (PAF) in cerebral ischemia-reperfusion injury, male Sprague-Dawley rats and albino mice of either sex were subjected to a 10-min bilateral carotid artery occlusion and 6-hr recirculation. The McGraw stroke index in mice was markedly inhibited by PAF antagonists, BN 52021 and CV 6209 (1 mg/kg, i.p., each) When they were administered 10 min before bilateral carotid artery occlusion or 1 hr after reperfusion. The increases in brain water content were significantly attenuated by treatment with BN 52021 or CV 6209 in both animals. BN 52021 exhibited a significant improvement in the postischemic blood pressure change in association with a beneficial effect on the delayed dilatation of pial arterioles after 10 min of ischemia. Thus it is suggested that PAF plays an important role as an endogenous mediator in development of cerebral ischemia-reperfusion injury, and further, specific antagonists to PAF will be able to prevent or reverse the pathological sequelae of cerebral ischemia.

• Biomedical Science Letters
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• v.11 no.3
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• pp.375-382
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• 2005

This study aimed to investigate whether nociceptin is implicated in the, trigeminovascular responses to electrical stimulation of trigeminal ganglion in rats. An open cranial window was prepared on the right parietal bone of male Sprague-Dawley rats. Trigeminovascular system was stimulated by electrical stimulation of trigeminal ganglion (ETS; 5ms, 5Hz, 3V). Neonatal capsaicin treatment was performed with subcutaneous administration of capsaicin (50mg/kg) within the first 24 hours after birth. Changes in regional cerebral blood flow were continuously measured through the cranial window by laser-Doppler flowmetry, and the expression of nociceptin-like immunoreactivity was determined by immunohistochemistry. ETS caused increases in regional blood flow of pial arteriole in a voltage-dependent manner. ETS markedly and voltage-dependently increased the expression of nociceptin-like immunoreactivity in dura mater ipsilateral rather than contralateral to ETS. The nociceptin-like immunoreactivity was markedly reduced by pretreatments with calcitonin gene-related peptide(8-37) ($CGRP_{8-37},\;a\;CGRP_1$ receptor antagonist), L-733060 (a $NK_1$ receptor antagonist), and $[Nphe^1]$ nociceptin(1-13)$NH_2$ (a selective and competitive nociceptin receptor antagonist) as well as by neonatal capsaicin treatment. These results suggest that the electrical stimulation of trigeminal ganglion causes prominent expression of nociceptin within dura mater, in which not only neuropeptides inducing substance P and CGRP but also nociceptin are implicated in the trigeminovascular responses to electrical trigeminal ganglion stimulation.