肝硬化患者血小板钙离子浓度变化及机制研究

Study on the mechanism and change of platelet[Ca^(2+)]_i in patients with hepatic cirrhosis

目的 探讨肝硬化患者血小板 [Ca2 + ] i 和甘氨脱氧胆酸 (GDCA)对血小板 [Ca2 + ] i 的影响。方法 荧光分光光度法测定肝硬化患者血小板 [Ca2 + ] i,以Fura2 /Am负载血小板 ,用甘氨脱氧胆酸作为处理因素 ,观察加入甘氨脱氧胆酸前后及不同浓度 ,不同时间 ,血小板 [Ca2 + ] i的变化。结果 ①肝硬化患者血小板 [Ca2 + ] i明显高于对照组 (P <0 0 1) ,上消化道出血组明显高于无出血组 (P <0 0 1)。②静息状态血小板 [Ca2 + ] i 为 5 8 74± 5 45 (n =3 ) ,在血小板处于无Ca2 +情况下 ,加入GDCA终浓度为 10 0 μmol/L时 ,随时间的延长血小板 [Ca2 + ] i 显著增加 ;GDCA终浓度分为 0、5 0、10 0、15 0、2 0 0 μmol/L时血小板 [Ca2 + ] i 随浓度增加而显著增加。血小板在有Ca2 + 环境下 (Ca2 + 终浓度为 1 3mmol/L) ,加入GDCA后 ,血小板 [Ca2 + ] i 随作用时间和GDCA浓度的增加而显著增加。结论 肝硬化患者血小板 [Ca2 + ] i 显著增加。GDCA能诱导血小板外Ca2 + 内流和内贮Ca2 + 释放 ,并与GDCA浓度和作用时间有关。肝硬化患者血小板 [Ca2 + ] i

Objective To investigate the mechanism and change of platelet [Ca 2+ ] i in patients with hepatic cirrhosis Methods Platelet [Ca 2+ ] i was measured and glycodeoxycholic acid(GDCA) was used to treat platelet,in order to investigate the change of platelet [Ca 2+ ] i in different time and in different concentrations of adding GDCA Results The platelet [Ca 2+ ] i in the patients with hepatic cirrhosis was significantly higher than that of normal controls( P <0 01),and it was also higher in gastrointestinal hemorrhage group than in non hemorrhage group( P <0 01) When GDCA was added with a final concentration of 100μmol/L without Ca 2+ in medium,Platelet [Ca 2+ ] i obviously increased with the time When GDCA was added with final concentrations 0,50,100,150,200 μmol/L respectively,platelet [Ca 2+ ] i significantly increased with the concentration of GDCA When Ca 2+ was present in medium with a concentration of 1 3mmol/L and GDCA had been added,platelet [Ca 2+ ] i obviously increased with the concentration of GDCA and the time Conclusion Platelet [Ca 2+ ] i greatly increased in patients with hepatic cirrhosis GDCA could induce the increase of [Ca 2+ ] i in platelet and the increase of Ca 2+ was due to not only extracellular Ca 2+ influx,but also intracellular stored Ca 2+ release Platelet [Ca 2+] i increase in patients with hepatic cirrhosis may be partly caused by bile acid