摘要
目的探讨蛋白激酶Ｃ（ＰＫＣ）活性变化在肺心病发病机制中的作用。方法用放免法测定１９例慢性肺心病急性发作期患者及２０名正常人血小板胞浆、胞膜ＰＫＣ活性，分析与动脉血氧分压（Ｐａｏ２）、动脉血二氧化碳分压（Ｐａｃｏ２）、血小板内游离钙离子浓度（［Ｃａ２＋］ｉ）之间相关关系。结果①肺心病组血小板胞浆ＰＫＣ活性明显低于对照组；血小板胞膜ＰＫＣ活性明显高于对照组（Ｐ＜００５，Ｐ＜００１）。②肺心病组Ｐａｏ２与血小板胞浆ＰＫＣ活性呈显著正相关（ｒ＝０．６０８，Ｐ＜００１）；与血小板胞膜ＰＫＣ活性呈显著负相关（ｒ＝－０．７５３，Ｐ＜００１）。结论肺心病患者存在血小板内ＰＫＣ被激活现象，活化的ＰＫＣ在肺心病发病机制中可能起着重要作用。缺氧是刺激ＰＫＣ活化的重要因素。
Objective\ To discuss the offect of protein kinase C
(PKC) activity on the pathogenests of cor pulmonale.Methods\ We measured the PKC activity in
platelet cytoplasm and memdrane by radioimmunoassay in 19 chronic cor pulmonale patients
in acute phase and 20 healthy people,and also studied the relationships bettween Pao 2、
Paco 2、platelet [Ca 2+ ]i and PKC activity in platelet cytoplasm and membrane.Results\ In
cor pulmonale group,platelet cytoplasm PKC activity significantly decreased ( P <0.05)、and
membrane PKC activity significantly increased ( P <0.01);There were significantly positive
correlation between Pao 2 and cytoplasm PKC activity (r=0.608、 P <0.01) and negative
correlation between Pao 2 and membrane PKC activity (r=-0.753、 P <0.01).Conclusions\
[WT5 BZ]PKC was activated in cor pulmonale patients and the activated PKC may have
important effect on the pathogenesis of cor pulmonale.Hypoxia may be the important factor that
stimulate PKC activation.
出处
《中国实用内科杂志》
CAS
CSCD
北大核心
1999年第5期291-292,共2页
Chinese Journal of Practical Internal Medicine
关键词
肺心病
血小板
蛋白激酶C
钙离子
Cor pulmonale\ Platelet\ Protein kinase C\ Intraplatelet free
calcium
