摘要
本前瞻性研究以外周红细胞作为心肌细胞的模型,动态观察(40d)8例心衰患者应用地高辛维持量疗法之红细胞洋地黄受体的数目、活性和泵单位活性的变化规律,并与8例未服用地高辛的心衰患者作平行对照。结果显示服用地高辛第3d洋地黄受体的活性与数目明显降低(p<0.01),尔后同步上升,20d后达服药前水平;停药后受体的活性与数目一度下降,第10d恢复到原有水平;而泵单位活性不变;红细胞洋地黄受体的活性与数目间有良好的正相关关系(r=0.9361,p<0.01)。提示红细胞洋地黄受体恢复到治疗前水平是继发于受体数目的增加,可能是导致地高辛正性肌力作用减弱甚至消失,即出现耐受的机理。明显的耐受性在连续服用地高辛20d左右形成,停药10d左右又恢复正常。
In this study, the dynamic changes in digitalis receptor activity(DRA), digitalis re-ceptor sites(DRS) and pump-unit activity(PUA) of peripheral intact erythrocytes, which were served as amodle of myocardial cells, from eight patients with heart failure were observed for 40 days during thedigoxin maintenance therapy. Meanwhile, other eight patients with heart failure were studied as a controlgroup during non-digoxin treatment. The results showed that DRA and DRS fell down significantly (p<0.01) on the third day of taking digoxin. Then, both DRA and DRS gradually increased and reached tothe pretreatment levels after the 20th day. They fell transiently on the third day (p<0.01) and then re-turned to the normal level on the 10th day of digoxin withdrawal. PUA. however, had no change duringdigoxin therapy and withdrawal. The linear correlation tests showed that there was a good positive corre-lation between DRA and DRS (r=0.9361, p<0.01). It suggested that the restore of DRA up to the pre-treatment level was secondary to the compensatory increase of DRS and might result in the decrease or evendisappearance of the positive inotropic effect of digoxin, which might be considered as the formation oftolerance to digoxin. Also, it was found that the significant tolerance was formed about on the 20th dayduring digoxin maintenance therapy and it took about 10 days after withdrawal for recovering to normal.At last it might be infered that'intermittence therapy' of digoxin would have a better clinical effect anddecrease the possibility of digitalis intoxication.
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
1993年第4期210-214,共5页
The Chinese Journal of Clinical Pharmacology
基金
陕西省科学技术发展计划项目(90KY-G8)
关键词
地高辛
洋地黄
受体
心力衰竭
digoxin receptor
digitalis
tolerance
sodium pump
heart failure
