烧伤后心肌细胞间隙连接通讯变化的机制研究

Changes of gap junctional intercellular communication in the myocardial cells and its mechanism after burns

目的：探讨烧伤后心肌细胞间隙连接通讯（Ｇａｐｊｕｎｃｔｉｏｎａｌｉｎｔｅｒｃｅｌｕｌａｒｃｏｍｍｕｎｉｃａｔｉｏｎ，ＧＪＩＣ）功能变化的病理生理机制。方法：采用缺氧、烧伤血清损伤培养心肌细胞模型，用划痕标记染料示踪技术检测ＧＪＩＣ功能，同时测定心肌细胞活力、胞浆游离钙及跨膜钙内流的变化。结果：缺氧及烧伤血清损伤后，心肌细胞活力明显降低，跨膜钙内流明显增加，同时伴胞浆游离钙浓度明显增加；正常心肌细胞培养后具有ＧＪＩＣ功能，ＬＹ荧光传递达划痕标记附近４列细胞。缺氧、缺氧加烧伤血清损伤后１ｈ即出现ＧＪＩＣ功能传导阻滞。缺氧６ｈ及缺氧加烧伤血清损伤３ｈ可出现荧光染料停滞在划痕线边沿细胞。结论：心肌ＧＪＩＣ功能保证心肌组织高度有序、同步收缩，烧伤后心肌细胞内钙稳态失控。

Objective: To understand the pathophysiological mechanism of the alteration of the myocardial cell gap junctional intercellular communication after burns. Methods: After the myocardial cells suffered from hypoxia were cultured with burn serum in vitro, the gap junctional intercelluarl communication was observed with crape loading and dye transferring. Meanwhile, the viability of and cytosolic free calcium ion concentration (Ca 2+ ) and Ca 2+ influx in the myocardial cells were also determined. Results: The LY fluorescence reached 4 rows of cells from the scraped line in the normal myocardial cells. The gap junctional intercellular communication was blocked at the 1st h after hypoxia, hypoxia and burn serum injury. The LY fluorescence was limited to the primary loading cells at the 6th h after hypoxia and at the 3rd h after hypoxia and burn serum injury. Conclusion: The function of gap junctional intercellular communication of the myocardial cells is to maintain high order synchronous contraction of the myocardial cells. After burns, the runaway calcium homeostasis and impairment of the gap junctional intercellular communication might contribute to the pathological basis of myocardial heterogeneous behavior.