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【目的】探讨T L R3基因在脓毒症心肌损伤中的作用及其机制。【方法】选择6周雄性野生型小鼠（野生型组）和TLR3基因敲除小鼠（基因敲除组），两组均采用盲肠结扎穿孔术（cecal ligation and puncture ，CLP）制作小鼠脓毒症模型，采用12 M Hz线阵超声探头评价两组建模前后心功能指标：心率（ HR）、左室舒／缩末期内径（LVEDD ，LVESD），左室前／后壁舒张末厚度（ Awd ，Pwd）、左心室收缩期前、后壁厚度（ Aws ，Pws）、左室短轴缩短率（ FS％）。两组建模48 h后动脉采血及分离左心室心肌，检测小鼠血清肌钙蛋白I（cTnI）和心肌匀浆上清液中肿瘤坏死因子‐α（TNF‐α）、内皮素‐1（ET‐1）浓度。【结果】野生型组小鼠建模后心功能明显变差，表现为左室舒、缩末期内径（L V EDD ，L V ESD ）显著增大（ P ＜0．05），FS％显著降低（ P ＜0．05）。建模后野生型组小鼠的TNF‐α和ET‐1因子在心肌浓度明显升高，且与血清cTnI 呈正相关，与 TLR3基因敲除组小鼠比较有统计学差异（ P ＜0．05）。【结论】TLR3基因是脓毒症心功能损伤的因素之一，其机制可能与炎症因子浸润心肌细胞有关。“,”[Objective] To explore the effects and mechanism of TLR3 gene in myocardial injury during sepsis .[Methods] Male wild‐type 6‐week‐old TLR3 knockout mice were divided into two groups .A 12 M Hz high‐fre‐quency linear array probe was employed for testing heart function by transthoracic echocardiography for two groups before and 48h after surgery .After 48h ,arterial blood samples were collected and left ventricular myocardium was isolated .And the serum concentration of cardiac troponin I (cTnⅠ) and the levels of tumor necrosis factor‐alpha (TNF‐α) and endothelin 1 (ET‐1) in myocardial homogenate supernatant were detected .[Results]After compa‐ring two groups before and after surgery ,cardiac function significantly worsened after surgery .Both left ventricu‐lar end diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) increased significantly ( P<0 .05) while fractional shortening (FS) declined significantly ( P < 0 .05) .TNF‐α and ET‐1 significantly in‐creased in myocardium after surgery and it was positively correlated with serum cTnI .And significant differences existed with TLR3 knockout mice group ( P <0 .05) .[Conclusion] TLR3 gene is one of factors for cardiac dys‐function during sepsis .And it may be due to an infiltration of inflammatory cytokines .