摘要
Objective: To explore the pathophysiological mechanism of the changes in gap junctionalintercellular communication (GJIC) in the myocardial cells after burns. Methods: After the myocardial cellswere cultured and injured with hypoxia and burn serum, the GJIC in the cells was detected with scrapeloading and dye transfer. Meanwhile, the viability, cytosolic free Ca2+ concentration and Ca2+ influx of themyocardial cells were determined. Results: The cytosolic free Ca2+ concentration and the cellulartransmembrane Ca2+ influx were significantly increased but the viability of the cells markedly decreased afterthe injury. The LY fluorescence reached 4 rows of cells from the scrape line in the normal myocardial cells.The GJIC was blocked at the first hour after hypoxia or hypoxia and burn serum injury. The LY fluorescencewas limited to the primary loads cells at the sixth hour after hypoxia and the third hour after hypoxia andburn serum injury. Conclusion: The function of GJIC in the myocardial cells is to maintain high ordersynchronous contraction of the myocardium. After burns, the runaway calcium homeostasis and impairmentof GJIC function would be accused to be the pathological basis for myocardial heterogeneous behavior.
Objective: To explore the pathophysiological mechanism of the changes in gap junctionalintercellular communication (GJIC) in the myocardial cells after burns. Methods: After the myocardial cellswere cultured and injured with hypoxia and burn serum, the GJIC in the cells was detected with scrapeloading and dye transfer. Meanwhile, the viability, cytosolic free Ca2+ concentration and Ca2+ influx of themyocardial cells were determined. Results: The cytosolic free Ca2+ concentration and the cellulartransmembrane Ca2+ influx were significantly increased but the viability of the cells markedly decreased afterthe injury. The LY fluorescence reached 4 rows of cells from the scrape line in the normal myocardial cells.The GJIC was blocked at the first hour after hypoxia or hypoxia and burn serum injury. The LY fluorescencewas limited to the primary loads cells at the sixth hour after hypoxia and the third hour after hypoxia andburn serum injury. Conclusion: The function of GJIC in the myocardial cells is to maintain high ordersynchronous contraction of the myocardium. After burns, the runaway calcium homeostasis and impairmentof GJIC function would be accused to be the pathological basis for myocardial heterogeneous behavior.
