• 제목/요약/키워드: Pial arteriole

검색결과 3건 처리시간 0.028초

토사자가 혈압(血壓), 국소뇌혈류량(局所腦血流量) 및 뇌연막동맥(腦軟膜動脈)에 미치는 영향(影響) (Effect of Cuscutae Semen Extract on Blood Pressure, Regional Cerebral Blood Flow and Pial Arterial Diameter in Rats)

  • 강성용;김경수;김경요;이인
    • 대한한의학방제학회지
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    • 제6권1호
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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.

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뇌의 허혈-재관류손상에 대한 연구: 혈소판활성인자의 관련 (A Study on Cerebral Ischemia-Reperfusion Injury: Involvement of Platelet-Activating Factor)

  • 이원석;임병용;홍기환
    • 대한약리학회지
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    • 제29권1호
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    • pp.1-8
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    • 1993
  • 뇌의 허혈-재관류 손상에 있어서 혈소판 활성인자 (PAF, platelet activating factor)의 관련을 증명하기 위하여 흰쥐와 생쥐에서 양측 총경동맥을 10분간 결찰하고 그후 6시간동안 재관류시켜 허혈-재관류 손상을 야기시켰다. 생쥐에 PAF 길항제인 BN52021과 CV6209 (각각 1 mg/kg, i.p.)를 총경동맥결찰 10분전 또는 재관류 시작 1시간 후에 투여시 McGram stroke index는 심하게 억제되었다. 흰쥐와 생쥐에서 뇌허혈-재관류에 의한 뇌수분함량의 증가는 BN52021 또는 CV6209 전처치에 의하여 유의하게 억제되었다. BN52021 전처치는 허혈 후의 혈압변동을 개선시켰을 뿐만 아니라 뇌연막동맥의 확장지연에 대하여도 효과가 있었다. 이러한 실험결과로 보아 PAF가 뇌허혈-재관류 손상의 발생에 내인성 인자로서 중요한 역할을 하는 것으로 사료된다. 나아가 PAF 길항제가 뇌허혈후의 병리학적 후휴증의 개선 내지는 예방에 사용 될 수 있을 것으로 기대된다.

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Expression of Nociceptin within Dura Mater in Response to Electrical Trigeminal Ganglion Stimulation in Rats

  • Kim, Jeong-Hee;Lee, Won-Suk
    • 대한의생명과학회지
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    • 제11권3호
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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.

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