前列腺素E1对舒张性心力衰竭病人血浆TNF的影响

The impact of prostandin E1 on tumor necrosis factors in blood of diastolic heart failure patients.

目的 观察前列腺素E1对舒张性心力衰竭病人血浆肿瘤坏死因子的影响。 方法 5 6名DHF患者随机分为两组 ,治疗组 2 8名 ,对照组 2 8名。治疗组用前列腺素E110 0 μg加入 5 %GS 2 5 0ml静脉滴注 ,1次 /d ,连用 3～ 4周 ;对照组用复方丹参注射液加入 5 %GS 2 5 0ml静脉滴注 ,1次 /d ,连用 3～ 4周。观察两组病人治疗前后血浆肿瘤坏死因子、左室舒张功能的有关参数以及有关常规指标的变化。 结果 两组病人治疗后心率较治疗前有所降低 (P <0 0 5 ) ,收缩压及舒张压 ,尿量治疗前后及两组间比较无显著性差异 (P >0 0 5 )。治疗组血浆TNF较治疗前明显降低 ,有统计学差异 (P <0 0 5 )。对照组血浆TNF治疗前后比较无明显统计学差异 (P >0 0 5 )。治疗后除X线心胸比值外 ,其余各项指标差别显著 (P <0 0 5 )。 结论 应用PGE1不仅有效改善心衰病人的舒张功能 ,同时伴有血浆TNF降低 ,说明PGE1可能通过阻止神经内分泌系统激活而抑制TNF的分泌是其治疗舒张性心力衰竭的机制之一。

Objective To observe the impact of prostandin E1 on tumor necrosis factors (TNF) in blood of diastolic heart failure (DHF) patients. Methods Fifty-six DHF patients were randomly divided into two groups, the treatment group and control group each consisted of 28 patients. The patients in treatment group were intravenously given 100μg prostandin E1 added into 250ml 5%GS one time per day, for 3～4 weeks; the patients in control group were also intravenously given fufangdansen injection added into 250ml 5%GS, one time per day for a consecutive of 3～4 weeks. Then the results were observed. Results The heart rates in the two groups were reduced after treatment than that before treatment (P<0.05); there were no differences in the systolic pressure, diastolic pressure, quantity of urine in the two groups before and after treatment (P>0.05). The blood TNF in the treatment group was obviously reduced after treatment (P<0.05). While no difference was found in the control group after treatment (P>0.05). Significant differences were noticed in other indexes (P<0.05) except cardiothoracic ratio of X-ray. Conclusion It shows that the application of prostandin E1 can not only improve the diastolic function of heart failure patients but can also reduce the blood TNF of the patients. One of the mechanism in the use of prostandin E1 for treatment of heart failure is that prostandin E1 may inhibit the secretion of TNF through preventing the activation of neuroendocrine system.