摘要
为探讨甘油三酯(TG)升高、高密度脂蛋白(HDL)降低与前列环素(PGI2)生物活性改变间的相互关系,选择65例高TG合并低HDL血症患者,以PGI2对二磷酸腺苷(ADP)诱导的血小板聚集的抑制率作为PGI2生物活性的指标,观察了其对PGI2生物活性的影响。结果发现,高TG合并低HDL血症时血小板聚集抑制率在10、20、50min时分别为(69.8±21.5)%、(47.5±25.0)%、(26.7±23.3)%,而对照组分别为(77.2±17.3)%、(60.7±26.1)%、(36.0±15.6)%,P<0.05或<0.01,表明高TG合并低HDL血症时对PGI2生物活性的稳定作用明显降低(P<0.01)。提示HDL对PGI2的稳定作用是由于其延长了PGI2的半寿期,而高TG血症可能通过使HDL降低而间接地影响PGI2的生物活性。
The influence of hypertriglyceridemia and low high density lipoprotein (HDL) on the PGI2 biological activity was studied in 65 patients. The rate of inhibition of PGI2 on ADP-induced platelet aggregation was used as the index of PGI2 biological activity. The results showed that the PGI2 biolngical activity in the group of low HDL was (69. 8±21. 5) %, (47. 5±25. 0) %, (26. 7±22. 3) 94, respectively at the time of 10, 20 and 50 minutes, significantly lower than that of the control group (P<0.05, <0.01 and <0.01 respectively), which was (77. 2±17.3) %, (60. 7±26.1) % and (36. 0±15. 6) %. The above findings suggest that the protection of HDL on PGI2 is due to the prolongation of PGI2 half life. Low HDL is considered as an important risk factor of coronary heart disease, there fore, impaired PGI2 biological activity and increased platelet aggregation might be one of the mechanisms.
出处
《同济医科大学学报》
CSCD
1997年第3期167-169,共3页
Acta Universitatis Medicinae Tongji
基金
国家自然科学基金!39170356