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作 者:唐法娣[1] 米原典史[1] 今井康夫 滝内■ 猪木令三 卞如濂
机构地区:[1]大阪大学齿学部药理学教室
出 处:《中国药理学报》1994年第3期232-234,共3页Acta Pharmacologica Sinica
摘 要:用放射免疫法测定缓激肽(BK)和P物质(SP)含量,发现正常大鼠(B/N-Ki)左后肢用47℃,热水刺激20 min,后肢足跖皮下灌流液中BK和SP含量分别为43±34和11.1±9.7fmol·min^(-1),比热刺激前显著增加,但在血浆激肽原缺乏大鼠(B/N-Ka),BK和SP含量分别为1.3±1.0和5.5±3.5fmol·min^(-1),明显低于B/N-Ki大鼠。B/N-Ka大鼠的E-vans蓝漏出量也低于B/N-Ki大鼠。表明热刺激时产生的BK可介导SP的释放。Contribution of kallikrein-kinin system to heat-induced substance P (SP) release into the periphery was studied by using plasma kininogens-deficient strain Brown Norway Katholiek (B/N-Ka) and normal strain Brown Norway Kitasato (B/N-Ki ) rats. Bradykinin (BK ) and SP levels in the sc per-fusates of the hind instep were measured by radioimmunoassay. In B/N-Ki rat, immersion of hind paw into hot water (47 ℃) for 20 min led to an increase of BK (43±s 34 fmol · min-1) and SP (11. 1±9. 7 fmol · min-1) in the perfusate, whereas those in B/N-Ka rat (BK 1. 3±1. 0 fmol · min-1 (P<0. 01), SP 5. 5±3. 5 fmol · min-1 (P<0. 05)) were remarkably less. Heat-induced extravasation (leakage of Evans blue) in B/N-Ka rat was also less than that in B/N-Ki rat (P<0. 05). Results suggest that kallikrein-kinin system is involved in the release of SP into the periphery, ie, BK released into the extravascular space by noxious heat stimulation intervenes in SP release.
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