Belch J J, O'Dowd A, Forbes C D, Sturrock R D
Br J Rheumatol. 1985 Nov;24(4):346-50. doi: 10.1093/rheumatology/24.4.346.
Vascular prostacyclin (PGI2) regulates platelet function and blood flow. In systemic sclerosis (SS) there is increased platelet aggregation (PA) but no information is available on the platelet/PGI2 relationship. We evaluated platelet sensitivity to a PGI2 analogue ZK36374 in 17 SS patients and 18 controls. The percentage (%) inhibition of PA was measured at two doses of ZK36374 with saline giving the 100% baseline. In the SS group 2 ng ZK36374 produced a percentage inhibition of 19 + 14 compared to a control value of 60 + 21, and 3 ng a percentage inhibition of 47 + 21 in the SS group and 82 + 20 in the controls. In 11 SS patients treated with either prostaglandin E or nifedipine the sensitivity approached normal. These data suggest that SS platelets are less sensitive to the inhibitory effect of PGI2 on PA. This may contribute to the vascular lesions of SS. Other cells are resistant to the effects of PGI2 and our findings support this picture of cellular resistance.
血管前列环素(PGI2)调节血小板功能和血流。在系统性硬化症(SS)中,血小板聚集(PA)增加,但关于血小板/PGI2关系的信息尚无。我们评估了17例SS患者和18例对照者对PGI2类似物ZK36374的血小板敏感性。以生理盐水作为100%基线,在两种剂量的ZK36374下测量PA的抑制百分比(%)。在SS组中,2 ng ZK36374产生的抑制百分比为19 + 14,而对照组的值为60 + 21;3 ng时,SS组的抑制百分比为47 + 21,对照组为82 + 20。在11例接受前列腺素E或硝苯地平治疗的SS患者中,敏感性接近正常。这些数据表明,SS患者的血小板对PGI2对PA的抑制作用较不敏感。这可能导致SS的血管病变。其他细胞对PGI2的作用也有抗性,我们的发现支持了这种细胞抗性的情况。