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前列腺素:对血小板黏附于胶原蛋白的特异性抑制及其与环磷酸腺苷水平的关系。

Prostaglandins: specific inhibition of platelet adhesion to collagen and relationship with cAMP level.

作者信息

Karniguian A, Legrand Y J, Caen J P

出版信息

Prostaglandins. 1982 Apr;23(4):437-57. doi: 10.1016/0090-6980(82)90108-3.

Abstract

The effect of 3 prostaglandins (PG's) (I2, D2 and E1) on the adhesion of platelets to purified type III collagen has been investigated. A quantitative method for a specific evaluation of the adhesion has been applied and has revealed an inhibition of adhesion by low concentrations (10(-10)M) of PGs added before collagen; the effect varied as a function of the dose of PGs (maximum at 10(-6)M) which also induced an increase in the level of platelet cAMP. The inhibition of adhesion and the elevation of platelet cAMP followed the same time course and were either of short duration (rapid decrease in the induced effects after 15 and 45 seconds in the case of PGE1) or longer lasting (maximum effect maintained for 5 minutes in the case of PGI2 and D2). These effects were potentiated by a phosphodiesterase inhibitor such as theophylline (10(-3)M). The addition of PGs after collagen resulted in a reduction of the enhancement of cAMP, associated with a decrease in the inhibition of adhesion. Moreover, the addition of exogenous cAMP (dibutyryl N6-02' cAMP) induced a comparable inhibition. A correlation between the adhesion of platelets to collagen and the level of either endogenous or exogenous cAMP has been established. The PGs also inhibited the platelet release reaction from the alpha granules (beta TG) and the dense bodies. (5-HT and ADP). A greater inhibition of release than of adhesion was observed for the same doses of PGs added.

摘要

研究了3种前列腺素(PGs)(I2、D2和E1)对血小板与纯化III型胶原黏附的影响。应用了一种用于特异性评估黏附的定量方法,结果显示在胶原之前添加低浓度(10⁻¹⁰M)的PGs可抑制黏附;其作用随PGs剂量而变化(在10⁻⁶M时最大),该剂量还可使血小板cAMP水平升高。黏附的抑制和血小板cAMP的升高具有相同的时间进程,且持续时间要么较短(如PGE1在15秒和45秒后诱导效应迅速下降),要么持续时间较长(如PGI2和D2的最大效应可维持5分钟)。这些效应可被磷酸二酯酶抑制剂如茶碱(10⁻³M)增强。在胶原之后添加PGs会导致cAMP增强的降低,同时黏附抑制作用减弱。此外,添加外源性cAMP(二丁酰N6 - O2' cAMP)会诱导类似的抑制作用。已确定血小板与胶原的黏附与内源性或外源性cAMP水平之间存在相关性。PGs还抑制了血小板从α颗粒(β - TG)和致密体(5 - HT和ADP)的释放反应。对于相同剂量的添加PGs,观察到其对释放的抑制作用大于对黏附的抑制作用。

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