CAJ | 학술논문

目的：观察慢性心力衰竭患者入院前后血浆偶联因子6( CF6)水平的动态变化。方法随机入选60例慢性心衰患者,根据心功能分级情况,按照指南规定提供标准化治疗,于入院即刻及入院后第5、10、14天分别测定血浆CF6及前列环素( PGI2)变化水平,观察慢性心衰患者经过治疗后,其CF6及PGI2的变化情况。结果慢性心力衰竭患者组入院时血浆CF6水平明显高于正常对照组,而PGI2水平明显降低,两组比较差异有统计学意义(P<0．01)。随着入院后治疗的进行,心衰各组CF6水平较入院时下降,且在不同时间点出现显著性差异,PGI2逐渐上升,且随着培哚普利剂量的增加,其下降或上升趋势更为明显。结论 CF6参与了慢性心力衰竭的病理生理过程,培哚普利通过纠正心衰患者血液动力学、改善内皮细胞功能等途径抑制CF6释放,提高PGI2,达到治疗心衰、改善患者预后的目的。
목적：관찰만성심력쇠갈환자입원전후혈장우련인자6( CF6)수평적동태변화。방법수궤입선60례만성심쇠환자,근거심공능분급정황,안조지남규정제공표준화치료,우입원즉각급입원후제5、10、14천분별측정혈장CF6급전렬배소( PGI2)변화수평,관찰만성심쇠환자경과치료후,기CF6급PGI2적변화정황。결과만성심력쇠갈환자조입원시혈장CF6수평명현고우정상대조조,이PGI2수평명현강저,량조비교차이유통계학의의(P<0．01)。수착입원후치료적진행,심쇠각조CF6수평교입원시하강,차재불동시간점출현현저성차이,PGI2축점상승,차수착배타보리제량적증가,기하강혹상승추세경위명현。결론 CF6삼여료만성심력쇠갈적병리생리과정,배타보리통과규정심쇠환자혈액동역학、개선내피세포공능등도경억제CF6석방,제고PGI2,체도치료심쇠、개선환자예후적목적。
Objective To observe the dynamical expression of the plasma coupling factor 6(CF6)levels in pa-tients with chronic heart failure( CHF) before and after admission and effects of perindopril on the factors. Methods All 60 patients with CHF were selected at random. The standardized treatment was provided according to the regulations of the guideline based on the grade of cardiac function. The plasma levels of CF6 and prostacyclin( PGI2 ) were deter-mined in all patients on immediate admission and 5,10,14 days after admission. The dynamic change of the plasma fac-tors were compared before and after the treatment. Results The plasma CF6 levels immediately after admission in pa-tients with CHF were significantly higher and the PGI2 levels were obviously lower than those of control group ( P<0. 05) . The CF6 levels gradually decreased along with the increase of the PGI2 levels after the treatment and there was significant difference at different time points. The trends became obvious with the increased dosage of perindopril. Con-clusion CF6 might involve in the pathophysiologic course of CHF. Perindopril can inhibit the release of plasma CF6 and elevate the PGI2 levels thus treat patients with CHF and improve prognosis by means of correcting the hemodynam-ics and improving endothelial cell function in patients with heart failure.