目的 观察低温缺氧/复氧（hypothermia hypoxia/reoxygen，H/R）后大鼠心肌成纤维细胞（rat cardiac fibroblasts，RCFs）对心肌 H9c2 细胞间通讯的影响并探讨其可能机制。方法 将 RCFs 细胞与 H9c2 细胞以 2:1 数量比 Transwell 共培养后随机分为 6 组。其中 T+AngⅡ组及 H/R⁃T+AngⅡ组加入 1.5 nmol/L Ang Ⅱ，T+ARB 组及 H/R⁃T+ARB 组加入 1 nmol/L 缬沙坦。T 组、T+AngⅡ组及 T+ARB 组进行正常培养，H/R⁃T 组、H/R⁃T+AngⅡ及 H/R⁃T+ARB 组进行 H/R 处理。检测各组培养液中 AngⅡ含量；H9c2 细胞 Cx43、ERK1/2 表达量及磷酸化及细胞间通讯情况。结果 与 T 组相比，H/R⁃T 组及 T+AngⅡ组 H9c2 细胞 ERK1/2、Cx43 表达及磷酸化水平降低（P < 0.05），细胞间通讯减弱（P < 0.05）；T+ARB 组 H9c2 细胞 ERK1/2、Cx43 表达及 磷酸化水平增高（P < 0.05），细胞间通讯增强（P < 0.05）。与 H/R⁃T 组相比，H/R⁃T+AngⅡ组 H9c2 细胞 ERK1/2、Cx43 表达及磷酸化水平降低（P < 0.05），细胞间通讯减弱（P < 0.05）；H/R⁃T+ARB 组 H9c2 细胞 ERK1/2、Cx43 表达及磷酸化水平增加（P < 0.05），细胞间通讯增强（P < 0.05）。结论 H/R 处理后，RCFs 细胞分泌增多的AngⅡ可能通过抑制H9c2细胞MAPK/ERK 通路下调Cx43表达，导致H9c2细胞间通讯减弱。

Objective To observe the effect on myocardial H9c2 cells gap junction intercellular communi⁃ cation（GJIC）by rat cardiac fibroblasts（RCFs）after hypothermia hypoxia/reoxygen（H/R）and to explore the pos⁃ sible mechanisms. Methods After co⁃cultured of RCFs cells with H9c2 cells in a 2:1 number ratio by Transwell， cells was randomly divided into 6 groups. The T+AngⅡ group and H/R⁃T+AngⅡ group were added 1.5nM AngⅡ， and the T+ARB group and H/R⁃T+ARB group were added 1nM valsartan. The T group，T+AngⅡ group and T+ ARB group were cultured normally，and the H/R⁃T group，H/R⁃T+AngⅡ and H/R⁃T+ARB group were treated with H/R. The AngⅡ concentration in the culture medium；the expression and phosphorylation of Cx43 and ERK1/2； and GJIC of H9c2 cells were detected. Results Compared with the T group，the expression and phosphorylation of ERK1/2 and Cx43 were decreased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in the H/R⁃T and T+Ang II group; he expression and phosphorylation of ERK1/2 and Cx43 were increased（P < 0.05）and GJIC was enhanced（P < 0.05）in H9c2 cells in the T+ARB group. Compared with H/R ⁃T group，he expression and phosphorylation of ERK1/2 and Cx43 were decreased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in H/R ⁃T+Ang II group; and the expression and phosphorylation of ERK1/2 and Cx43 were increased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in H/R ⁃T+ARB group. Conclusion After H/R，in⁃ creased AngⅡ secretion by RCFs may downregulate Cx43 expression by inhibiting the MAPK/ERK pathway in H9c2 cells，resulting in diminished GJIC between H9c2 cells.