Objectiv e It is to observe the effect of Shenmai injection on myocardial calmodulin ( CaM) and cardiac tropo-nin I (CTNI) and their gene expression in patients with acute myocardial infarction with cardiogenic shock , and to explore the mechanism of its improvement of cardiac pump function .Methods One hundred and sixty-four patients with cardiogenic shock after acute myocardial infarction were randomly divided into conventional treatment group and Shenmai group , the conventional therapy group was given emergency conventional therapy for cardiogenic shock after acute myocardial infarction , Shengmai group was added with Shenmai injection 60 mL by intravenous drip additionally on the basis of treatment in control conventional group.The changes of CaM and CTNI and their gene expression , cardiac pump function, urine volume, HR, BP before and after treatment were observed in both groups , the clinical curative effect , complications and mortality rate was compared .Re-sults After 7 days’ treatment, compared with conventional treatment group , the serum levels of CTNI and CTNIm-RNA, CaM and CaMKII-mRNA and pulmonary capillary wedge pressure (PCWP),left ventricular systolic diameter (LVESD) and end-diastolic interventricular septum thickness (IVST)were significantly lower(P<0.05), while left ventricular maximum rise/fall rate ( ± LV dp/dtmax), left ventricular ejection fraction (LVEF), left ventricular end diastolic diameter (LVEDD), di-astolic blood pressure (DP) and differential pulse pressure (PP), urine volume and cardiac index (CI) were higher in Shen-mai injection than those in conventional treatment group (P<0.05).The total effective rate was higher, the occurrence rate of complications and mortality rate was lower in Shenmai injection group than those in conventional therapy group (P<0.05). Conclusion Shengmai injection can enhance cardiac pump function in the patients after acute myocardial infarction with cardio -genic shock , its mechanism should be associated with down-regulating CTNI and CaM ,correcting abnormal open of calcium channels , avoiding calcium overload in myocardial cells .%目的：观察生脉注射液对急性心肌梗死后心源性休克患者心肌肌钙蛋白I （cTNI）和心肌钙调蛋白（ CaM）及其基因表达的影响，探讨其增强患者心脏泵功能的机制。方法将164例急性心肌梗死后心源性休克急诊患者随机均分为常规治疗组和生脉组，常规治疗组给予急性心肌梗死后心源性休克急诊常规用药处理，生脉组在此治疗基础上给予生脉注射液60 mL静滴。观察2组治疗前后心肌相关蛋白及其基因表达情况及心脏泵功能、尿量、心率和血压变化情况，统计2组临床疗效、并发症发生情况及病死率。结果治疗7d后，与常规治疗组比较，生脉组血清cTNI 和cTNI mRNA、CaM 和钙调蛋白依赖性蛋白激酶Ⅱ（CaMKⅡ）mRNA水平及肺毛细血管楔压（PCWP）均明显降低（P均＜0．05），左心室收缩末期内径（LVESD）和舒张末期室间隔厚度（IVST）缩小，左心室最大上升／下降速率（±LV dp／dtmax）、左心室射血分数（LVEF ）、左心室舒张末内径（LVEDD）、舒张压（DBP）和脉压差（PP）增大（P均＜0．05），尿量和心脏指数（CI）明显增加（P均＜0．05）。生脉组总有效率明显高于常规治疗组（P均＜0．05），室间隔穿孔、心律失常和急性肾衰竭发生率及病死率均明显低于常规治疗组（P均＜0．05）。结论生脉注射液可增强急性心肌梗死后心源性休克患者心脏泵功能，机制可能与其下调cTNI和CaM、纠正异常开放的钙通道、避免心肌细胞“钙超载”有关。
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