CAJ | 학술논문

目的：探讨基因重组促红细胞生成素(r-HuEPO)在治疗慢性肾衰(CRF)贫血中导致高血压的机制及防治对策。方法：对r-HuEPO治疗中出现高血压CRF血液透析贫血患者15例及对照组15例，CRF贫血动物模型，以及透析过程中出现低血压的34例患者，应用分光光度法及放免法观察用药或透析前后血浆一氧化氮(NO)代谢产物(N02-/NO3-)及内皮素-1(ET-1)的变化。结果：①CRF贫血患者及贫血鼠用r-HuEPO治疗16周后，红细胞压积(Hct)升高，血压升高，ET-1升高(P＜0.01)，血浆NO2-/N03-下降(P＜0.01)，而对照组用药前后无明显变化(P＞0.05)。②在用药16周后，RT-PCR测得实验组大鼠肾皮质及髓质iNOSmRNA比对照组明显减少(P＜0.05)。③透析低血压患者透析后NO2-/NO3-含量增高，ET-1含量减少(P＜0.05)。结论：研究表明r-HuEPO导致高血压与iNOSmRNA减少、合成NO减少和ET-1增加有重要的关系。
목적：탐토기인중조촉홍세포생성소(r-HuEPO)재치료만성신쇠(CRF)빈혈중도치고혈압적궤제급방치대책。방법：대r-HuEPO치료중출현고혈압CRF혈액투석빈혈환자15례급대조조15례，CRF빈혈동물모형，이급투석과정중출현저혈압적34례환자，응용분광광도법급방면법관찰용약혹투석전후혈장일양화담(NO)대사산물(N02-/NO3-)급내피소-1(ET-1)적변화。결과：①CRF빈혈환자급빈혈서용r-HuEPO치료16주후，홍세포압적(Hct)승고，혈압승고，ET-1승고(P＜0.01)，혈장NO2-/N03-하강(P＜0.01)，이대조조용약전후무명현변화(P＞0.05)。②재용약16주후，RT-PCR측득실험조대서신피질급수질iNOSmRNA비대조조명현감소(P＜0.05)。③투석저혈압환자투석후NO2-/NO3-함량증고，ET-1함량감소(P＜0.05)。결론：연구표명r-HuEPO도치고혈압여iNOSmRNA감소、합성NO감소화ET-1증가유중요적관계。
Objective: To investigate the pathogenesis of r-HuEPO-related hypertension. Methods: Changes of nitric oxide(NO) production and endothelin-l(ET-1) were observed in anemic patients with chronic renal failure (CRF) during hemodial-vsis (HD),anemic rats with CRF after 16 weeks of r-HuEPO treatment resulting in hypertension and control groups. We alsodid the similar detection in patients with hypertension during HD. The levels of plasma NO metabolites (NO2-/NO3- ) and ET-1 were determined. Then inducible NO synthase mRNA (iNOS mRNA) was detected by RT-PCR in rats' renal cortical andmedulla. Results: Hct,BP and the levels of plasma ET-1 were significantly higher(P＜0.01),but the levels of plasma NOwere markedly lower ( P＜0.05 ). There were no changes of these in control groups ( P＞0.05). Othermore, the level of plasmaNO2-/NO3- was increased and ET-1 was decreased after HD iNOS mRNA level was obviously lower in CRF rats than that ofcontrol rats. Conclusion: The decreases of iNOS mRNA and the increases of ET-1 play an important role in the development ofhypertension relating to r-HuEPO therapy.