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探讨βＡ４２５－３５的血管活性作用的机制，为Ａｌｚｈｅｉｍｅｒ病的发病提供理论依据。方法采用大鼠皮肤水疱模型，使用内皮素拮抗剂ＢＱ－１２３（１０μｍｏｌ）及蛋白激酶Ｃ抑制剂ｂｉｓｉｎｄｏｌｙｌｍａｌｅｉｍｉｄｅ（ＢＩＭ，１μｍｏｌ）分别在灌注βＡ４２５－３５之前及同时进行灌注。使用激光多普勒血流计监测血流变化。结果同时灌注ＢＱ－１２３和βＡ４２５－３５或ＢＩＭ和βＡ４２５－３５完全消除了βＡ４２５－３５的ＶＣ反应，此后再灌注Ｐ物质诱导出正常的ＶＤ反应。结论在皮肤微循环水平，内皮素和蛋白激酶Ｃ在βＡ４２５－３５诱导的血管活性反应中起着重要作用。
To explore the mechanism of βA425-35 vasoactive effect, provide a theoretical basis for the pathogenesis of Alzheimer’s disease. Methods Rat skin blister model was used. Perfusion was performed before and concurrently with βA425-35 by using endothelin antagonist BQ-123 (10μmol) and protein kinase C inhibitor bisindolylmaleimide (BIM, 1μmol). Laser Doppler flowmeters were used to monitor changes in blood flow. Results Simultaneous perfusion of BQ-123 and βA425-35 or BIM and βA425-35 completely abolished the VC response of βA425-35 and subsequent reperfusion of substance P induced a normal VD response. Conclusions Endothelin and protein kinase C play an important role in βA425-35 induced vasoreactivity at the level of skin microcirculation.