心先安对充血性心力衰竭患者左室收缩功能的影响及机制的初步探讨

The Effects and Mechanisms of Meglumine Cyclicadenylate on LeftVentricular Systolic Function in Patients with Congestive Heart Failure

为研究心先安对充血性心力衰竭患者左室收缩功能的影响及其机制，采用超声心动图法对患者治疗前后的左室收缩功能作了评定，并观察了心先安对培养乳鼠心肌细胞内环磷酸腺苷（ｃＡＭＰ） 及乳酸脱氢酶（ＬＤＨ） 漏出的影响。３４ 例病人随机分成２ 组：常规治疗组和心先安治疗组，疗程均为１ 周。治疗后心先安组ＬＶＥＤＤ 缩短（ 从６３ ．９ ±１０ ．５ 到５９ ．０ ±１１ ．６ ｍ ｍ ，Ｐ＜ ０ ．０１） ，ＬＶＥＳＶ 减小（ 从１３９ ．７ ±２９ ．０ 到１１１ ．２ ±２３ ．０ｍｌ，Ｐ＜ ０ ．０５） ，ＬＶＥＦ（ ％ ） 提高（ 从３８ ．９ ±１２ ．３ 到４５ ．７ ±１４ ．５ ，Ｐ＜ ０ ．０１）ＳＶ、ＣＯ、ＣＩ增加（ 分别从６１ ．７ ±２２ ．５到８５ ．１ ±２６ ．３ ｍｌ，从５ ．２ ±１ ．６ 到６ ．６ ±２ ．４１／ｍｉｎ，从２ ．６ ±０ ．４ 到４ ．０ ±１ ．１ １／ｍｉｎ／ｍ２ ，均为Ｐ＜ ０ ．０５） 。常规治疗组治疗前后的改变无统计学显著意义。心先安能增加培养的乳心鼠肌细胞内ｃＡＭＰ 浓度，呈剂量依赖性，并能减少缺氧／ 复氧损伤心肌细胞ＬＤＨ 的漏出，亦呈剂量依赖性。结果显示，心先安能改善心力衰竭患者的左室收缩功能，其机制可能与升高细胞内ｃＡＭＰ?

In order to study the effects of meglumine cyclicadenylate(MCA) on the systolic function of left ventricle and its mechanisms in patients with congestive heart failure,the left ventriicular systolic function was meassured with echocardiography before and after treatment,effects on the concentration of cyclic adenosine monophosphate(cAMP) and leakage of intracellular lactate dehydrogenase(LDH) in cultured neonatal rat cardiomyocytes were investigated.Thirty four patients were involved in this study and randomly assigned to two groups:(1) the routine therapy group;(2) the MCA therapy group,both groups were treated for one week.LVEDD(mm) shorted from 63 9±10.5 to 59.0±11.6( P <0.01),LVESV(ml) decreased from 139.7±29.0 to 112.2±23.0( P <0 05),LVEF(%) elevated from 38.9±12.3 to 45.7±13.5( P <0.01),SVCOCI all increased(from61.7±22.5 to 85 1±26.3 ml,from 5.2±1.6 to 6.6±2.4 l/min,from 2.6±0.4 to 4.0±1.1 l/min/m 2respectively,all P <0 05)in MCA group.The changes in routine therapy group were no significance.MCA increased the concentration of intracellular cAMP in a concentration dependent manner and lowcred the leakage of intracellualr LDH in anoxia/reoxygenation injury group also in a concentration dependent manner.The results indicated that MCA could improve the left ventricular systolic function in patients with congestive heart failure and the mechanism possibly included the effects of increased the concentration of intracellular cAMP and protective on cardiomyocytes anoxia injury.